PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16962210-1 2006 The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Tritium 62-64 angiotensinogen Rattus norvegicus 100-114 16962210-2 2006 Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. Tritium 24-31 angiotensinogen Rattus norvegicus 0-14 16962210-4 2006 Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Tritium 37-44 angiotensinogen Rattus norvegicus 0-14 15501693-10 2004 [3H] Ang II binding at AT1 receptors was unaltered in vascular smooth muscle membranes prepared from thoracic aorta exposed to HG for 2 h compared to NG exposed aortic rings. Tritium 1-3 angiotensinogen Rattus norvegicus 5-11 17111039-6 2006 Ang II enhanced [3H]-leucine incorporation, beta-MHC mRNA expression, PKC activity, and PKCepsilon expression and inhibited alpha-MHC mRNA expression in cardiomyocytes. Tritium 17-19 angiotensinogen Rattus norvegicus 0-6 21162229-4 2006 RESULTS: Angiotensin II caused a significant increase in MTT value and 3H-TdR uptake in CNM, which could be significantly reversed by pioglitazone and 15d-PGJ2 in a dose-dependent manner. Tritium 71-73 angiotensinogen Rattus norvegicus 9-23 21166160-7 2005 RESULTS: Pioglitazone inhibited ANP and BNP mRNA expression and 3H-leucine incorporation in neonatal rat cardiac myocytes induced by angiotensin II in a dose-dependent manner in vitro. Tritium 64-66 angiotensinogen Rattus norvegicus 133-147 17079869-4 2006 Here we report that catechin, epicatechin (EC), epicatechingallate (ECG) or epigallocatechingallate (EGCG) significantly inhibits the Ang II-induced [3H]thymidine incorporation into the primary cultured rat aortic VSMC. Tritium 150-152 angiotensinogen Rattus norvegicus 134-140 17079869-7 2006 U0126, a MEK inhibitor, SP600125, a JNK inhibitor, or SB203580, a p38 inhibitor, attenuates the Ang II-induced [3H]thymidine incorporation into the VSMC. Tritium 112-114 angiotensinogen Rattus norvegicus 96-102 16297473-4 2006 Injections of ANG-II for 5-days caused significant increase of the 3H-thymidine labeling index (M+/-m) in the myocardium of 7-day-old rats (from 6.95+/-0.32% to 8.53+/-0.22%, p<0.05). Tritium 67-69 angiotensinogen Rattus norvegicus 14-20 16380538-5 2006 [3H]-thymidine and [3H]-proline incorporation by cardiac fibroblasts treated with Ang II was enhanced when the cells were pretreated with AICAR. Tritium 1-3 angiotensinogen Rattus norvegicus 82-88 16380538-5 2006 [3H]-thymidine and [3H]-proline incorporation by cardiac fibroblasts treated with Ang II was enhanced when the cells were pretreated with AICAR. Tritium 20-22 angiotensinogen Rattus norvegicus 82-88 14693677-10 2004 Inhibition of PI3K, using the selective inhibitor LY-294002, and downregulation of SAM68, by antisense oligonucleotides, significantly decreased ANG II-stimulated incorporation of [3H]leucine and [3H]thymidine in VSMCs, showing the functional significance of PI3K and SAM68. Tritium 181-183 angiotensinogen Rattus norvegicus 145-151 15226216-4 2004 Ang II-induced myocyte hypertrophy assessed by increments in cell size, [3H]leucine uptake, and protein content was suppressed by HO-1 overexpression. Tritium 73-75 angiotensinogen Rattus norvegicus 0-6 14693677-10 2004 Inhibition of PI3K, using the selective inhibitor LY-294002, and downregulation of SAM68, by antisense oligonucleotides, significantly decreased ANG II-stimulated incorporation of [3H]leucine and [3H]thymidine in VSMCs, showing the functional significance of PI3K and SAM68. Tritium 197-199 angiotensinogen Rattus norvegicus 145-151 14985098-4 2004 [3H]Thymidine incorporation assay revealed that Ang II enhanced DNA synthesis in PSCs, which was blocked by Ang II type 1 receptor antagonist losartan. Tritium 1-3 angiotensinogen Rattus norvegicus 48-54 15127886-5 2004 In contrast, incubation of SMC for 48 h with angiotensin II (AII, 100 nmol/l) resulted in a significant increase in the cell size measured by flowcytometric forward-angle light scatter assay, in association with an increase in the ratio of [3H]leucine/[3H]thymidine uptake, indicating SMC hypertrophy. Tritium 241-243 angiotensinogen Rattus norvegicus 45-59 15127886-5 2004 In contrast, incubation of SMC for 48 h with angiotensin II (AII, 100 nmol/l) resulted in a significant increase in the cell size measured by flowcytometric forward-angle light scatter assay, in association with an increase in the ratio of [3H]leucine/[3H]thymidine uptake, indicating SMC hypertrophy. Tritium 241-243 angiotensinogen Rattus norvegicus 61-64 15127886-5 2004 In contrast, incubation of SMC for 48 h with angiotensin II (AII, 100 nmol/l) resulted in a significant increase in the cell size measured by flowcytometric forward-angle light scatter assay, in association with an increase in the ratio of [3H]leucine/[3H]thymidine uptake, indicating SMC hypertrophy. Tritium 253-255 angiotensinogen Rattus norvegicus 45-59 15127886-5 2004 In contrast, incubation of SMC for 48 h with angiotensin II (AII, 100 nmol/l) resulted in a significant increase in the cell size measured by flowcytometric forward-angle light scatter assay, in association with an increase in the ratio of [3H]leucine/[3H]thymidine uptake, indicating SMC hypertrophy. Tritium 253-255 angiotensinogen Rattus norvegicus 61-64 14985098-4 2004 [3H]Thymidine incorporation assay revealed that Ang II enhanced DNA synthesis in PSCs, which was blocked by Ang II type 1 receptor antagonist losartan. Tritium 1-3 angiotensinogen Rattus norvegicus 108-114 14647975-3 2003 Angiotensin II (30-1,000 nM) and bradykinin (10-300 nM) enhanced the evoked overflow of tritium, the maximum increase reaching 52.2 and 72.8%, respectively. Tritium 88-95 angiotensinogen Rattus norvegicus 0-14 14704121-6 2004 RESULTS: In cardiac myocyte Ang II increased p44/p42 MAPK activity and phosphorylated protein content by 140 % and 699 %, and also increased [3H]leucine incorporation and cell diameter by 40 % and 27 %. Tritium 142-144 angiotensinogen Rattus norvegicus 28-34 21179843-2 2002 We also investigated the effect of MKP-1 genes,which were transfected into vascular smooth muscle cells (VSMC) using the classical calcium phosphate coprecipitation technique, on the incorporation of 3H-TdR in VSMC stimulated by angiotensin II (Ang II). Tritium 200-202 angiotensinogen Rattus norvegicus 229-243 21179843-7 2002 In the transfected cells with wild MKP-1 gene, Ang II-induced incorporation of 3H-TdR lowered 63%, compared with untransfected cells (P < 0.05). Tritium 79-81 angiotensinogen Rattus norvegicus 47-53 12941780-6 2003 In hearts from citrate-treated control rats, angiotensin II-stimulated [(3)H]phenylalanine incorporation and atrial natriuretic peptide and beta-myosin heavy chain mRNA expression were prevented by B-type natriuretic peptide (BNP), bradykinin, the ACE inhibitor ramiprilat, and the neutral endopeptidase inhibitor candoxatrilat. Tritium 72-76 angiotensinogen Rattus norvegicus 45-59 12398914-3 2002 Angiotensin II (10-300 nM) and bradykinin (3-100 nM) enhanced the evoked overflow of tritium, the maximum increase reaching 63.2% and 87.1%, respectively. Tritium 85-92 angiotensinogen Rattus norvegicus 0-14 12167494-6 2002 Although STS (10 microM) alone showed no effect on the growth of cultured cardiac cells, it markedly suppressed angiotensin II-induced enlargement of cells and [3H]phenylalanine incorporation, proceeding from the induction of immediate early gene (c-jun) expression in myocytes. Tritium 161-163 angiotensinogen Rattus norvegicus 112-126 12054679-8 2002 Finally, Ang II-induced [3H]leucine incorporation into RASMC was abolished by Q3GA. Tritium 25-27 angiotensinogen Rattus norvegicus 9-15 21179843-6 2002 (2) 3H-TdR incorporation in VSMC stimulated by Ang II (10(-7) mol/L) was increased by 207% (P < 0.01), compared with control group. Tritium 4-6 angiotensinogen Rattus norvegicus 47-53 11181554-5 2001 In rat prostate, Ang II (0.01-1 microM) produced a concentration-dependent increase in [(3)H]-noradrenaline release from sympathetic nerves. Tritium 87-93 angiotensinogen Rattus norvegicus 17-23 11530112-6 2001 RESULTS: ANG II induced a dose-dependent decrease of DNA-synthesis in BAEC measured by [3H]-thymidine incorporation. Tritium 88-90 angiotensinogen Rattus norvegicus 9-15 11749808-9 2001 Que (1-100 micromol/L) could inhibit the increase of total protein content, incorporation of [14C]uridine and [3H]tyrosine, and PKC and TPK activities induced by Ang II in concentration-dependent manner. Tritium 110-114 angiotensinogen Rattus norvegicus 162-168 12585075-7 2001 Tet (0.1-10 mumol.L-1) treatment in vitro induced a concentration dependent depression [3H]-proline incorperation stimulated by NE or Ang II in AVSMCs from either Sham or RHR. Tritium 88-90 angiotensinogen Rattus norvegicus 134-140 12899339-6 2001 Cyclosporin A(CsA), a specific inhibitor of calcineurin, markedly inhibited the calcineurin activity and decreased the 3H-leucine incorporation in AngII-treated cardiomyocytes in a dose-dependent manner. Tritium 119-121 angiotensinogen Rattus norvegicus 147-152 28095237-4 2001 Stimulation with Ang II (100 nM), ET-1 (100 nM) or PE (1 microM) induced marked increases in [3H]Leucine incorporation (>= 50%), compatible with enhanced protein synthesis. Tritium 94-96 angiotensinogen Rattus norvegicus 17-23 11041248-5 2000 Ang II, Ang III and CV-11974 completely displaced the [3H]DuP753 binding with slope factors near unity, but PD123319 did not. Tritium 55-57 angiotensinogen Rattus norvegicus 0-6 11369814-6 2001 Ang II-induced [3H]leucine incorporation was reduced in a dose-dependent way by torasemide (IC(50) value: 7.7+/-0.8x10(-7) M) but not by furosemide. Tritium 16-18 angiotensinogen Rattus norvegicus 0-6 11062338-5 2000 However, the two peptides significantly attenuated the angiotensin II-induced [3H]thymidine incorporation in the smooth muscle cells. Tritium 79-81 angiotensinogen Rattus norvegicus 55-69 11133011-7 2000 Sarpogrelate also significantly attenuated angiotensin-II- and endothelin-1-induced [3H]-leucine uptake. Tritium 85-87 angiotensinogen Rattus norvegicus 43-57 11073110-1 2000 We have shown that losartan, a selective inhibitor of AT1 receptors for angiotensin II (AII), inhibits the binding of [3H]fMLP to neutrophil receptors (FPR). Tritium 119-121 angiotensinogen Rattus norvegicus 72-86 11073110-1 2000 We have shown that losartan, a selective inhibitor of AT1 receptors for angiotensin II (AII), inhibits the binding of [3H]fMLP to neutrophil receptors (FPR). Tritium 119-121 angiotensinogen Rattus norvegicus 88-91 11041248-2 2000 [3H]Ang II binding to the membrane fractions exhibited both high (Kd =0.08 nm, Bmax =2.19 fmol/mg protein) and low (Kd =4.19 nm, Bmax = 13.7 fmol/mg protein) affinity. Tritium 1-3 angiotensinogen Rattus norvegicus 4-10 11041248-3 2000 Ang 11, Ang III and saralasin completely displaced the [3H]Ang II binding, whereas CV-11974, an AT1 receptor antagonist and PD123319, an AT2 receptor antagonist maximally displaced up to approximately 87 and 13% of the total binding, respectively. Tritium 56-58 angiotensinogen Rattus norvegicus 8-14 10987999-3 2000 The influence of isoprenaline, the compound CGS21680 and angiotensin II on the overflow of tritium evoked by electrical stimulation was checked before and after alpha(2)-adrenoceptor blockade. Tritium 91-98 angiotensinogen Rattus norvegicus 57-71 10987999-4 2000 All the agonists used caused concentration-dependent increases of tritium overflow, the maximal effect representing increases of 44.2, 27.4 and 41.2% for isoprenaline, CGS21680 and angiotensin II, respectively. Tritium 66-73 angiotensinogen Rattus norvegicus 181-195 10952156-6 2000 Cultured cardiac myocytes treated with Ang II and infected with either control or recombinant adenovirus indicated that expression of p21 and p16 inhibited Ang II-induced cardiac myocyte hypertrophy, [3H]leucine incorporation into total cellular proteins, and skeletal alpha-actin (SK-A) and atrial natriuretic peptide (ANP) mRNA accumulation. Tritium 201-203 angiotensinogen Rattus norvegicus 156-162 10888262-3 2000 Angiotensin II (1 microM) induced a 34 +/- 2% increase in [3H]phenylalanine incorporation (P<0.001), an in vitro marker of hypertrophy, in adult rat cardiomyocytes co-cultured with bovine aortic endothelial cells. Tritium 59-61 angiotensinogen Rattus norvegicus 0-14 10810318-7 2000 Finally, using [(3)H]methylthymidine uptake as an index of cellular proliferation, tritium incorporation was increased in the AII-treated group at concentrations greater than 10(-10) M. The aldosterone antagonist, spironolactone (10(-5) M), inhibited the incorporation of [(3)H]thymidine into RASMCs stimulated by AII. Tritium 83-90 angiotensinogen Rattus norvegicus 126-129 10810318-7 2000 Finally, using [(3)H]methylthymidine uptake as an index of cellular proliferation, tritium incorporation was increased in the AII-treated group at concentrations greater than 10(-10) M. The aldosterone antagonist, spironolactone (10(-5) M), inhibited the incorporation of [(3)H]thymidine into RASMCs stimulated by AII. Tritium 83-90 angiotensinogen Rattus norvegicus 314-317 10907723-5 1999 When AngII was included in the buffer, evoked [3H]overflow increased in a concentration-dependent manner in ISBAT slices from AngII-infused and control rats. Tritium 47-49 angiotensinogen Rattus norvegicus 5-10 10523380-6 1999 In the P-ECM, Ang II was the only factor that produced a lesser effect on [(3)H]-glucosamine and a greater effect on [(35)S]-sodium sulfate uptakes in VSMC from SHR than from Wistar rats. Tritium 74-80 angiotensinogen Rattus norvegicus 14-20 11270995-7 1999 DNA synthesis and collagen protein synthesis induced by Ang II for 24 h were measured by [3H]thymidine incorporation and [3H]Proline incorporation, respectively. Tritium 90-92 angiotensinogen Rattus norvegicus 56-62 11270995-7 1999 DNA synthesis and collagen protein synthesis induced by Ang II for 24 h were measured by [3H]thymidine incorporation and [3H]Proline incorporation, respectively. Tritium 122-124 angiotensinogen Rattus norvegicus 56-62 10615423-6 1999 Synthetic AM significantly reduced 10(-6) mol/l Ang II- or 10(-7) mol/l ET-1-stimulated [3H]thymidine and [3H]phenylalanine incorporation in a dose-dependent manner, and these effects were attenuated by a calcitonin gene-related peptide (CGRP) type 1 receptor antagonist, CGRP(8-37). Tritium 89-91 angiotensinogen Rattus norvegicus 48-54 10405778-6 1999 In myocytes cocultured with normal BAEC, angiotensin II (AngII; 1 mumol/L) significantly increased [3H]-phenylalanine incorporation (an in vitro marker of hypertrophy) by 32 +/- 2%. Tritium 100-102 angiotensinogen Rattus norvegicus 41-55 10405778-6 1999 In myocytes cocultured with normal BAEC, angiotensin II (AngII; 1 mumol/L) significantly increased [3H]-phenylalanine incorporation (an in vitro marker of hypertrophy) by 32 +/- 2%. Tritium 100-102 angiotensinogen Rattus norvegicus 57-62 10087056-7 1999 However, it caused a 40-50% attenuation of the Ang II-induced increase in norepinephrine transporter (NET) and tyrosine hydroxylase (TH) mRNAs and [3H]-NE uptake in the SHR neuron. Tritium 148-150 angiotensinogen Rattus norvegicus 47-53 10907723-4 1999 Using superfused ISBAT tissue slices preloaded with [3H]norepinephrine (NE), evoked [3H]overflow was greater in ISBAT slices from AngII-infused rats compared to controls. Tritium 53-55 angiotensinogen Rattus norvegicus 130-135 11498949-2 1999 The results showed that angiotensin II induced c-fos mRNA expression, increased protein content in a dose-dependent manner and stimulated 3H-leucine incorporation rate. Tritium 138-140 angiotensinogen Rattus norvegicus 24-38 10615423-6 1999 Synthetic AM significantly reduced 10(-6) mol/l Ang II- or 10(-7) mol/l ET-1-stimulated [3H]thymidine and [3H]phenylalanine incorporation in a dose-dependent manner, and these effects were attenuated by a calcitonin gene-related peptide (CGRP) type 1 receptor antagonist, CGRP(8-37). Tritium 107-109 angiotensinogen Rattus norvegicus 48-54 9746487-2 1998 Angiotensin II increased [3H]phenylalanine incorporation by 21 +/- 2% in myocytes cocultured with endothelial cells; this was abolished by bradykinin in the presence of endothelial cells. Tritium 26-28 angiotensinogen Rattus norvegicus 0-14 9746487-5 1998 Angiotensin II also increased [3H]phenylalanine incorporation by 28 +/- 3% in myocytes cultured in the absence of endothelial cells. Tritium 31-33 angiotensinogen Rattus norvegicus 0-14 10907723-5 1999 When AngII was included in the buffer, evoked [3H]overflow increased in a concentration-dependent manner in ISBAT slices from AngII-infused and control rats. Tritium 47-49 angiotensinogen Rattus norvegicus 126-131 9845003-3 1998 The effect of AngII (20% inhibition) on [3H]GABA release was decreased by the addition of 0.01 mM nipecotic acid to the superfusion medium. Tritium 41-43 angiotensinogen Rattus norvegicus 14-19 9845003-4 1998 AngII also decreased the Ca2+-independent carrier-mediated [3H]GABA release (25% inhibition at a concentration of 1 microM). Tritium 60-62 angiotensinogen Rattus norvegicus 0-5 9845003-2 1998 Angiotensin II (AngII) at a concentration of 1 microM inhibited K+-stimulated [3H]GABA release. Tritium 79-81 angiotensinogen Rattus norvegicus 0-14 9740613-9 1998 Inhibition of MAP kinase by either an MAP kinase kinase inhibitor (PD98059) or an MAP kinase antisense oligonucleotide completely attenuated the stimulatory effects of Ang II on [3H]-NE uptake, NE transporter mRNA, and tyrosine hydroxylase mRNA levels in WKY neurons. Tritium 179-181 angiotensinogen Rattus norvegicus 168-174 9845003-2 1998 Angiotensin II (AngII) at a concentration of 1 microM inhibited K+-stimulated [3H]GABA release. Tritium 79-81 angiotensinogen Rattus norvegicus 16-21 9740614-9 1998 Further studies showed that the degree of insulin-mediated [3H]thymidine uptake in VSMCs could be duplicated by 4x10(-10) mol/L Ang II. Tritium 60-62 angiotensinogen Rattus norvegicus 128-134 9740614-10 1998 Losartan reduced the effects of both Ang II and insulin on [3H]thymidine uptake by about 40% to 45% of baseline (P<0.05). Tritium 60-62 angiotensinogen Rattus norvegicus 37-43 9260984-10 1997 Ang II (10(-7) mol/L) increased DNA ([3H]thymidine incorporation) and protein synthesis ([3H]leucine incorporation). Tritium 38-40 angiotensinogen Rattus norvegicus 0-6 9727550-7 1998 TNF-alpha (10 ng/mL) and Ang II (100 nmol/L) enlarged cardiac myocytes and increased [3H]leucine uptake, and BHA (10 micromol/L) significantly inhibited both effects. Tritium 86-88 angiotensinogen Rattus norvegicus 25-31 9667070-3 1998 The density of [3H]-Ang II binding to renal tissue was concentration-dependent in both renal cortex and medulla. Tritium 16-18 angiotensinogen Rattus norvegicus 20-26 9667070-4 1998 Although the addition with 500 nM arginine vasopressin and 500 nM atrial natriuretic peptide had no effect on [3H]-Ang II, the total binding of [3H] Ang II completely displaced by the addition with 500 nM unlabeled Ang II or L-158,809. Tritium 145-147 angiotensinogen Rattus norvegicus 149-155 9667070-4 1998 Although the addition with 500 nM arginine vasopressin and 500 nM atrial natriuretic peptide had no effect on [3H]-Ang II, the total binding of [3H] Ang II completely displaced by the addition with 500 nM unlabeled Ang II or L-158,809. Tritium 145-147 angiotensinogen Rattus norvegicus 149-155 10375734-6 1998 Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1). Tritium 97-99 angiotensinogen Rattus norvegicus 13-27 10375734-6 1998 Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1). Tritium 97-99 angiotensinogen Rattus norvegicus 29-35 10375734-6 1998 Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1). Tritium 109-111 angiotensinogen Rattus norvegicus 13-27 10375734-6 1998 Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1). Tritium 109-111 angiotensinogen Rattus norvegicus 29-35 9736248-5 1998 Ang II increases intracellular inositol 1,4,5-triphosphate (IP3) and [Ca2+]i and stimulates [3H]thymidine incorporation and extracellular matrix (ECM) synthesis via AT1A receptors. Tritium 93-95 angiotensinogen Rattus norvegicus 0-6 9449388-11 1998 Angiotensin II increased [3H]phenylalanine incorporation by 24+/-3% in adult cardiomyocytes in monoculture and by 22+/-2% in adult rat cardiomyocytes cocultured with endothelial cells. Tritium 26-28 angiotensinogen Rattus norvegicus 0-14 9278099-4 1997 The [3H]Ang II binding to intact cells was inhibited by dithiothreitol (DTT), and the rank order of potency of Ang II and nonpeptide antagonists to inhibit the [3H]Ang II binding was Ang II > Losartan >> PD 123319 or CGP 42112B, indicating the presence of the AT1 receptor type. Tritium 5-7 angiotensinogen Rattus norvegicus 8-14 9278099-4 1997 The [3H]Ang II binding to intact cells was inhibited by dithiothreitol (DTT), and the rank order of potency of Ang II and nonpeptide antagonists to inhibit the [3H]Ang II binding was Ang II > Losartan >> PD 123319 or CGP 42112B, indicating the presence of the AT1 receptor type. Tritium 161-163 angiotensinogen Rattus norvegicus 8-14 9278099-4 1997 The [3H]Ang II binding to intact cells was inhibited by dithiothreitol (DTT), and the rank order of potency of Ang II and nonpeptide antagonists to inhibit the [3H]Ang II binding was Ang II > Losartan >> PD 123319 or CGP 42112B, indicating the presence of the AT1 receptor type. Tritium 161-163 angiotensinogen Rattus norvegicus 111-117 9278099-4 1997 The [3H]Ang II binding to intact cells was inhibited by dithiothreitol (DTT), and the rank order of potency of Ang II and nonpeptide antagonists to inhibit the [3H]Ang II binding was Ang II > Losartan >> PD 123319 or CGP 42112B, indicating the presence of the AT1 receptor type. Tritium 161-163 angiotensinogen Rattus norvegicus 111-117 9278099-4 1997 The [3H]Ang II binding to intact cells was inhibited by dithiothreitol (DTT), and the rank order of potency of Ang II and nonpeptide antagonists to inhibit the [3H]Ang II binding was Ang II > Losartan >> PD 123319 or CGP 42112B, indicating the presence of the AT1 receptor type. Tritium 161-163 angiotensinogen Rattus norvegicus 111-117 9278099-5 1997 Whereas most of the [3H]Ang II binding at 4 degrees was susceptible to acid or pronase treatment, binding at 35 degrees was resistant to both treatments, suggesting an internalization of the Ang II-receptor complex. Tritium 21-23 angiotensinogen Rattus norvegicus 24-30 9278099-8 1997 Chloroquine (100 microM) inhibited the [3H]Ang II dissociation from cells, and monensin (25 microM) induced a 30% inhibition of [3H]Ang II binding (35 degrees, 3 hr), suggesting endosomal processing of the Ang II-receptor complex with receptor recycling to the cell surface. Tritium 40-42 angiotensinogen Rattus norvegicus 43-49 9278099-8 1997 Chloroquine (100 microM) inhibited the [3H]Ang II dissociation from cells, and monensin (25 microM) induced a 30% inhibition of [3H]Ang II binding (35 degrees, 3 hr), suggesting endosomal processing of the Ang II-receptor complex with receptor recycling to the cell surface. Tritium 129-131 angiotensinogen Rattus norvegicus 132-138 9278099-8 1997 Chloroquine (100 microM) inhibited the [3H]Ang II dissociation from cells, and monensin (25 microM) induced a 30% inhibition of [3H]Ang II binding (35 degrees, 3 hr), suggesting endosomal processing of the Ang II-receptor complex with receptor recycling to the cell surface. Tritium 129-131 angiotensinogen Rattus norvegicus 132-138 9260984-10 1997 Ang II (10(-7) mol/L) increased DNA ([3H]thymidine incorporation) and protein synthesis ([3H]leucine incorporation). Tritium 90-92 angiotensinogen Rattus norvegicus 0-6 9281446-7 1997 However, in the presence of PD123319 Ang II stimulated [3H]leucine (+24%) and [3H]thymidine (+30%) incorporation. Tritium 56-58 angiotensinogen Rattus norvegicus 37-43 9281446-7 1997 However, in the presence of PD123319 Ang II stimulated [3H]leucine (+24%) and [3H]thymidine (+30%) incorporation. Tritium 79-81 angiotensinogen Rattus norvegicus 37-43 9281446-10 1997 Ang II stimulated [3H]leucine incorporation (+24%) in fibroblasts. Tritium 19-21 angiotensinogen Rattus norvegicus 0-6 9231818-7 1997 Interleukin-1 alpha treatment enhanced Ang II-induced [3H]uridine incorporation, whereas treatment with interleukin-1 alpha combined with tumor necrosis factor-alpha/interferon gamma attenuated Ang II-induced [3H]uridine and [3H]leucine incorporation. Tritium 55-57 angiotensinogen Rattus norvegicus 39-45 9231818-7 1997 Interleukin-1 alpha treatment enhanced Ang II-induced [3H]uridine incorporation, whereas treatment with interleukin-1 alpha combined with tumor necrosis factor-alpha/interferon gamma attenuated Ang II-induced [3H]uridine and [3H]leucine incorporation. Tritium 55-58 angiotensinogen Rattus norvegicus 39-45 9231818-7 1997 Interleukin-1 alpha treatment enhanced Ang II-induced [3H]uridine incorporation, whereas treatment with interleukin-1 alpha combined with tumor necrosis factor-alpha/interferon gamma attenuated Ang II-induced [3H]uridine and [3H]leucine incorporation. Tritium 210-212 angiotensinogen Rattus norvegicus 194-200 9255399-4 1997 ANG II induced a marked increase in 3H-thymidine incorporation in cultured vascular smooth muscle cells. Tritium 36-38 angiotensinogen Rattus norvegicus 0-6 8997162-7 1996 The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. Tritium 128-130 angiotensinogen Rattus norvegicus 52-58 8922747-7 1996 Angiotensin II (0.1-3 microM) produced concentration-dependent enhancement of both stimulation-induced (S-I) efflux of [3H]-noradrenaline and stimulation-evoked vasoconstrictor responses in isolated preparations of caudal artery from both SH and WKY rats, in which the noradrenergic transmitter stores had been labelled with [3H]-noradrenaline. Tritium 120-122 angiotensinogen Rattus norvegicus 0-14 8997162-8 1996 The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). Tritium 45-47 angiotensinogen Rattus norvegicus 4-10 8898348-6 1996 Treatment with nerve growth factor (NGF) induced an inhibition of [3H]thymidine incorporation, which was enhanced by ANG II, maximally 25% at the highest concentration. Tritium 67-69 angiotensinogen Rattus norvegicus 117-123 8898348-7 1996 The effects of ANG II on [3H]thymidine incorporation were reflected by those on cell number and were prevented by the AT2 receptor antagonist, PD123177, but not influenced by the AT1 receptor antagonist, losartan. Tritium 26-28 angiotensinogen Rattus norvegicus 15-21 8675248-4 1996 Ang-(1-7) inhibited [3H]thymidine incorporation in response to stimulation by fetal bovine serum, platelet-derived growth factor, or Ang II. Tritium 21-23 angiotensinogen Rattus norvegicus 133-139 8678895-3 1996 AII, platelet-derived growth factor-BB (PDGF-BB), and epidermal growth factor (EGF) caused a 3426 +/- 262%, 277 +/- 69%, and 1568 +/- 62% increase in [3H]thymidine incorporation in VSMC (mean +/- SD, n = 3), respectively. Tritium 151-153 angiotensinogen Rattus norvegicus 0-3 8675248-10 1996 The AT1 antagonist losartan or L-158,809 but not AT2 antagonists blocked [3H]thymidine incorporation by Ang II. Tritium 74-76 angiotensinogen Rattus norvegicus 104-110 8922747-16 1996 Rather, combinations of 0.1 microM angiotensin II and PD 123319 (both 0.01 and 0.1 microM) enhanced S-I [3H]-noradrenaline efflux, whereas 0.1 microM angiotensin II alone was without effect. Tritium 105-107 angiotensinogen Rattus norvegicus 35-49 8675248-8 1996 In contrast, Ang II stimulated [3H]thymidine incorporation in cultured vascular smooth muscle cells over the same concentration range, with a maximal stimulation of 314% at 1 mumol/L Ang II. Tritium 32-34 angiotensinogen Rattus norvegicus 13-19 8675248-8 1996 In contrast, Ang II stimulated [3H]thymidine incorporation in cultured vascular smooth muscle cells over the same concentration range, with a maximal stimulation of 314% at 1 mumol/L Ang II. Tritium 32-34 angiotensinogen Rattus norvegicus 183-189 8613266-9 1996 Ang II stimulated a mild but significant proliferation of quiescent cells, as measured by [3H]thymidine incorporation and direct cell counting. Tritium 91-93 angiotensinogen Rattus norvegicus 0-6 8834708-1 1996 The present study was designed to evaluate the effect of chronic treatment with losartan, an AT1 angiotensin II receptor antagonist, and enalaprilat, an angiotensin converting enzyme inhibitor, on the presynaptic modulation of [3H]-norepinephrine release from isolated atria of spontaneously hypertensive rats (SHR) and their respective control, the Wistar-Kyoto rats (WKY). Tritium 228-230 angiotensinogen Rattus norvegicus 97-111 8593828-4 1996 Ang II causes both acute and chronic stimulation of [3H]-norepinephrine (NE) uptake in neuronal cultures of Wistar Kyoto (WKY) rat brain. Tritium 53-55 angiotensinogen Rattus norvegicus 0-6 8593828-7 1996 Chronic stimulation of [3H]-NE uptake by Ang II persists throughout the duration of Ang II incubation (24 h), is dose dependent, and is also mediated by AT1 receptor subtype. Tritium 24-26 angiotensinogen Rattus norvegicus 41-47 8593828-7 1996 Chronic stimulation of [3H]-NE uptake by Ang II persists throughout the duration of Ang II incubation (24 h), is dose dependent, and is also mediated by AT1 receptor subtype. Tritium 24-26 angiotensinogen Rattus norvegicus 84-90 8593828-9 1996 Ang II also stimulates [3H]-NE uptake in neuronal cultures of SH rat brain, both acutely and chronically, by mechanisms similar to those observed in neuronal cultures of WKY rat brain. Tritium 24-26 angiotensinogen Rattus norvegicus 0-6 8577935-7 1995 Reports that [3H]losartan binds to a non-angiotensin II binding site in rat liver and in other tissues could be confirmed. Tritium 14-16 angiotensinogen Rattus norvegicus 41-55 7648260-2 1995 In the WKY rat, Ang II promoted a dose-dependent increase in the IC50 value of l-noradrenaline when competing for ([3H]p-aminoclonidine ([3H]PAC) binding sites, which reached a maximum of 400% with 10 nM of Ang II and was associated with a small decrease in the B0 value (20%). Tritium 116-118 angiotensinogen Rattus norvegicus 16-22 7573419-5 1995 CM from ANG II-treated NF enhanced [3H]Leu incorporation 2.2-fold in NM. Tritium 36-38 angiotensinogen Rattus norvegicus 8-14 7635942-4 1995 Both ET-1 and ANG II significantly stimulated [3H] thymidine incorporation into cardiac fibroblasts, whose effects were dose-dependently inhibited by an ETA receptor antagonist (BQ123), BQ123 also inhibited both ET-1- and ANG II-induced ppET-1 mRNA expression. Tritium 47-49 angiotensinogen Rattus norvegicus 14-20 7635942-5 1995 Both atrial and brain natriuretic peptides (ANP, BNP), which activate particulate guanylate cyclase, inhibited ppET-1 mRNA expression and [3H]thymidine incorporation stimulated by ANG II and ET-1. Tritium 139-141 angiotensinogen Rattus norvegicus 180-186 7660676-7 1995 Ang II increased [3H] thymidine uptake without demonstrable mitogenic activity. Tritium 18-20 angiotensinogen Rattus norvegicus 0-6 7660676-8 1995 Lovastatin inhibited PDGF (10 ng/ml in mesangial cell, 25 ng/ml in smooth muscle cell)-, ET (10(-7)M)- and Ang II (10(-7)M)-induced [3H] thymidine uptake significantly in a dose-dependent manner in both cells. Tritium 133-135 angiotensinogen Rattus norvegicus 107-113 7648260-2 1995 In the WKY rat, Ang II promoted a dose-dependent increase in the IC50 value of l-noradrenaline when competing for ([3H]p-aminoclonidine ([3H]PAC) binding sites, which reached a maximum of 400% with 10 nM of Ang II and was associated with a small decrease in the B0 value (20%). Tritium 116-118 angiotensinogen Rattus norvegicus 207-213 7648260-4 1995 Saturation analysis also showed that Ang II (0.1 nM) increased the KD value of [3H]PAC in the WKY strain but in contrast decreased the KD value of [3H]PAC in the SHR. Tritium 80-82 angiotensinogen Rattus norvegicus 37-43 7648260-4 1995 Saturation analysis also showed that Ang II (0.1 nM) increased the KD value of [3H]PAC in the WKY strain but in contrast decreased the KD value of [3H]PAC in the SHR. Tritium 148-150 angiotensinogen Rattus norvegicus 37-43 7670738-2 1995 We show here that angiotensin II (AII) and endothelin-1 (ET-1) stimulate [3H]-thymidine incorporation in a smooth muscle cell line derived from aortae of spontaneously hypertensive rats (SHR), but not in cells derived from normotensive controls (WKY). Tritium 74-76 angiotensinogen Rattus norvegicus 18-32 7670738-2 1995 We show here that angiotensin II (AII) and endothelin-1 (ET-1) stimulate [3H]-thymidine incorporation in a smooth muscle cell line derived from aortae of spontaneously hypertensive rats (SHR), but not in cells derived from normotensive controls (WKY). Tritium 74-76 angiotensinogen Rattus norvegicus 34-37 7670738-13 1995 Stimulation of SHR-derived cells with 100 nM AII for 1 h, followed by 19 h in the absence of agonist, stimulated [3H]-thymidine incorporation over the next 4 h. When the 1 h stimulation with AII was in the presence of increasing concentrations of butanol, which diverts the product of the phospholipase D pathway, there was a loss of stimulated [3H]-thymidine incorporation which was significant at 10 mM butanol and at 30-50 mM reached a maximum loss of 40%. Tritium 114-116 angiotensinogen Rattus norvegicus 45-48 7670738-13 1995 Stimulation of SHR-derived cells with 100 nM AII for 1 h, followed by 19 h in the absence of agonist, stimulated [3H]-thymidine incorporation over the next 4 h. When the 1 h stimulation with AII was in the presence of increasing concentrations of butanol, which diverts the product of the phospholipase D pathway, there was a loss of stimulated [3H]-thymidine incorporation which was significant at 10 mM butanol and at 30-50 mM reached a maximum loss of 40%. Tritium 114-116 angiotensinogen Rattus norvegicus 191-194 7670738-13 1995 Stimulation of SHR-derived cells with 100 nM AII for 1 h, followed by 19 h in the absence of agonist, stimulated [3H]-thymidine incorporation over the next 4 h. When the 1 h stimulation with AII was in the presence of increasing concentrations of butanol, which diverts the product of the phospholipase D pathway, there was a loss of stimulated [3H]-thymidine incorporation which was significant at 10 mM butanol and at 30-50 mM reached a maximum loss of 40%. Tritium 346-348 angiotensinogen Rattus norvegicus 45-48 7670738-13 1995 Stimulation of SHR-derived cells with 100 nM AII for 1 h, followed by 19 h in the absence of agonist, stimulated [3H]-thymidine incorporation over the next 4 h. When the 1 h stimulation with AII was in the presence of increasing concentrations of butanol, which diverts the product of the phospholipase D pathway, there was a loss of stimulated [3H]-thymidine incorporation which was significant at 10 mM butanol and at 30-50 mM reached a maximum loss of 40%. Tritium 346-348 angiotensinogen Rattus norvegicus 191-194 7556269-9 1995 However, for endothelium-denuded organoids, medial [3H]-thymidine incorporation in the combined presence of Ang II and cilazaprilat was not significantly different from that in untreated controls. Tritium 52-54 angiotensinogen Rattus norvegicus 108-114 7621917-4 1995 CV-11974 and TCV-116 inhibited the angiotensin II-induced increase in [3H]thymidine incorporation with an IC50 of 3 x 10(-10) and 5 x 10(-9) M, respectively. Tritium 71-73 angiotensinogen Rattus norvegicus 35-49 7952881-9 1994 The selective AT2 receptor ligand, CGP 42112A, antagonized AII-induced [3H]-thymidine incorporation with an IC50 of 6.3 +/- 1.3 microM while the AT2/AT1B receptor antagonist, PD 123319, was found to be almost inactive (IC50 > 10 microM). Tritium 72-74 angiotensinogen Rattus norvegicus 59-62 7556269-6 1995 Inclusion of 10(-7) M Ang II significantly elevated medial [3H]-thymidine incorporation above that in control cultures. Tritium 60-62 angiotensinogen Rattus norvegicus 22-28 8574778-3 1995 When 10 nM ANF was added to the medium containing KCl plus ANG II or KCl plus ANG III, the reduction of 3H-NE output by ANF was greater than when the atrial factor was added to the medium containing only ANG II or ANG III. Tritium 104-106 angiotensinogen Rattus norvegicus 59-65 8574778-3 1995 When 10 nM ANF was added to the medium containing KCl plus ANG II or KCl plus ANG III, the reduction of 3H-NE output by ANF was greater than when the atrial factor was added to the medium containing only ANG II or ANG III. Tritium 104-106 angiotensinogen Rattus norvegicus 78-84 7952881-4 1994 In cultured rat aortic vascular smooth muscle (VSMC), exposure to AII (0.1 to 100 nM) resulted in a concentration-dependent increase in [3H]-thymidine incorporation with an EC50 of 1.41 +/- 0.51 nM. Tritium 137-139 angiotensinogen Rattus norvegicus 66-69 7952881-5 1994 Maximal stimulation was observed in the presence of 100 nM AII and corresponded to 271 +/- 40% of basal [3H]-thymidine incorporation. Tritium 105-107 angiotensinogen Rattus norvegicus 59-62 7952881-8 1994 The stimulatory effect of AII (3 nM) on [3H]-thymidine incorporation in VSMC was antagonized by the non-selective AT1/AT2 receptor antagonist, [Sar1, Ile8]-AII (IC50 = 5.6 nM), by the AT1A/AT1B receptor antagonist, losartan (IC50 = 10.5 nM) and the AT1 receptor antagonist, L-158809 (IC50 = 0.20 nM). Tritium 41-43 angiotensinogen Rattus norvegicus 26-29 7952881-8 1994 The stimulatory effect of AII (3 nM) on [3H]-thymidine incorporation in VSMC was antagonized by the non-selective AT1/AT2 receptor antagonist, [Sar1, Ile8]-AII (IC50 = 5.6 nM), by the AT1A/AT1B receptor antagonist, losartan (IC50 = 10.5 nM) and the AT1 receptor antagonist, L-158809 (IC50 = 0.20 nM). Tritium 41-43 angiotensinogen Rattus norvegicus 156-159 7859394-6 1995 The rate of [3H]phenylalanine incorporation into cardiac proteins was 3.9-fold (P < .005) and 2.6-fold (P < .01) higher in angiotensin II-perfused (n = 6) than in vehicle-perfused (n = 6) left and right ventricles, respectively. Tritium 13-15 angiotensinogen Rattus norvegicus 129-143 8156919-11 1994 When tested with [3H]corticosterone and [3H]progesterone as exogenous substrates, 1-10 microM cotinine caused a significant dose-dependent inhibition of ACTH- and ANG-II-stimulated aldosterone synthesis. Tritium 18-20 angiotensinogen Rattus norvegicus 163-169 8156919-11 1994 When tested with [3H]corticosterone and [3H]progesterone as exogenous substrates, 1-10 microM cotinine caused a significant dose-dependent inhibition of ACTH- and ANG-II-stimulated aldosterone synthesis. Tritium 41-43 angiotensinogen Rattus norvegicus 163-169 8160786-7 1994 Only treatment of mesangial cells by ANG II or EXP-3174 produced downregulation of [3H]losartan binding sites. Tritium 84-86 angiotensinogen Rattus norvegicus 37-43 8166267-5 1994 ANG II increased evoked 3H overflow in ISBAT slices to a greater extent in preobese rats compared with control. Tritium 24-26 angiotensinogen Rattus norvegicus 0-6 8166267-10 1994 ANG II did not increase evoked 3H overflow in obese rats; however, ANG II increased evoked 3H overflow in lean rats. Tritium 91-93 angiotensinogen Rattus norvegicus 67-73 7509348-3 1994 In 24-h [3H]-thymidine incorporation assays, AII was found to be a weak mitogen when compared to potent mitogens such as fetal bovine serum and platelet-derived growth factor (PDGF). Tritium 9-11 angiotensinogen Rattus norvegicus 45-48 8118839-3 1994 Treatment of growth-arrested (in 0.4% fetal calf serum) cells with platelet-derived growth factor (0.3-7.5 nM) or angiotensin II (0.001-1000 nM) induced 3H-thymidine incorporation and cell proliferation in a dose-dependent manner (P < 0.01). Tritium 153-155 angiotensinogen Rattus norvegicus 114-128 8279541-3 1993 Additionally, in ISF slices preloaded with [3H]norepinephrine (NE), ANG II (10 nM) resulted in an increase (3-fold) in evoked 3H overflow from ISF slices from cold-exposed rats compared with ambient temperature controls. Tritium 44-46 angiotensinogen Rattus norvegicus 68-74 7734113-3 1994 AII increased evoked [3H] overflow from slices from control rats. Tritium 22-24 angiotensinogen Rattus norvegicus 0-3 7734113-5 1994 Acute losartan administration inhibited AII-induced enhancement of evoked [3H]overflow. Tritium 75-77 angiotensinogen Rattus norvegicus 40-43 8279541-6 1993 Administration of the non-peptide AT1-receptor antagonist losartan to cold-exposed rats resulted in complete inhibition of ANG II-mediated presynaptic facilitation of evoked 3H overflow from ISF slices. Tritium 174-176 angiotensinogen Rattus norvegicus 123-129 1338078-7 1992 Incubation of quiescent cells with 0.1 mumol/l angiotensin II resulted in a 65% increase in total [3H]-inositol phosphates released compared with unstimulated cells and in a rapid accumulation of c-fos messenger RNA (mRNA). Tritium 99-101 angiotensinogen Rattus norvegicus 47-61 8240422-0 1993 Angiotensin II and non-angiotensin II displaceable binding sites for [3H]losartan in the rat liver. Tritium 70-72 angiotensinogen Rattus norvegicus 0-14 8240422-0 1993 Angiotensin II and non-angiotensin II displaceable binding sites for [3H]losartan in the rat liver. Tritium 70-72 angiotensinogen Rattus norvegicus 23-37 8240422-1 1993 By virtue of the more than 1000-fold selectivity of losartan (DuP 753) for the AT1 angiotensin II (AII) receptor subtype compared with the AT2 subtype, [3H]losartan may be a useful radioligand for studies of the AT1 receptor subtype. Tritium 153-155 angiotensinogen Rattus norvegicus 83-97 8240422-3 1993 In addition, AII at concentrations as high as 10 microM displaced less than one-third of specific [3H]losartan binding in the liver and less than 80% in the whole adrenal. Tritium 99-101 angiotensinogen Rattus norvegicus 13-16 8240422-4 1993 The presence of non-AII displaceable [3H]losartan binding in the liver did not appear to result from metabolism of the radioligand since HPLC analysis of free and bound 3H revealed that greater than 90% of the 3H eluted at the same time as the parent [3H]losartan. Tritium 38-40 angiotensinogen Rattus norvegicus 20-23 8282008-3 1993 In comparison, [3H][Sar1,Ala8]angiotensin II binding sites exhibited the same KD value (4.3 nM), but a considerably lower Bmax (52 fmol/mg protein). Tritium 16-18 angiotensinogen Rattus norvegicus 30-44 8111824-8 1993 Binding to ANGII receptors was determined in brain sections incubated with 3 nM [125I]Sar1 ANGII, exposed to [3H]Hyperfilm with an optical density of autoradiograms measured by computerized densitometry. Tritium 110-112 angiotensinogen Rattus norvegicus 11-16 8326007-7 1993 ET-1 and ANG II stimulated twofold increase [3H]leucine incorporation into cardiomyocytes, whose effects were similarly and dose dependently inhibited by endothelin A receptor antagonist (BQ123). Tritium 45-47 angiotensinogen Rattus norvegicus 9-15 8326007-8 1993 Introduction of antisense sequence against coding region of ppET-1 mRNA into cardiomyocytes resulted in complete blockade with ppET-1 mRNA levels and [3H]leucine incorporation stimulated by ANG II. Tritium 151-153 angiotensinogen Rattus norvegicus 190-196 8469770-3 1993 The present studies were designed to ascertain which receptor subtype mediates three AngII-induced physiologic functions in rat mesangial cells namely intracellular Ca2+ mobilization, adenylyl cyclase inhibition and protein synthesis as monitored via [3H]leucine incorporation. Tritium 252-254 angiotensinogen Rattus norvegicus 85-90 8234032-0 1993 Binding of [3H]angiotensin II and [3H]DuP 753 (Losartan) to rat liver homogenates reveals multiple sites. Tritium 12-14 angiotensinogen Rattus norvegicus 15-29 8234032-3 1993 Competition experiments with human angiotensin I, II, and III and with the angiotensin antagonists, CGP 42114A, saralasin, DuP 753, and PD123177, confirmed that the [3H]angiotensin II binding was to an AT1-type receptor. Tritium 166-168 angiotensinogen Rattus norvegicus 169-183 8234032-10 1993 Saturation studies using both angiotensin II and DuP 753 to define nonspecific binding showed that [3H]DuP 753 bound to at least two types of site, one smaller population of receptors that was sensitive to both angiotensin II and DuP 753 and a second site that was sensitive to DuP 753 only. Tritium 100-102 angiotensinogen Rattus norvegicus 211-225 1508302-9 1992 Angiotensin II stimulated [3H]InsP3 was increased (219%) in old rats. Tritium 27-29 angiotensinogen Rattus norvegicus 0-14 1480133-0 1992 Characterization of the binding of [3H]L-158,809: a new potent and selective nonpeptide angiotensin II receptor (AT1) antagonist radioligand. Tritium 36-38 angiotensinogen Rattus norvegicus 88-102 1480133-1 1992 [3H]L-158,809, a new potent and AT1-selective nonpeptide angiotensin II receptor antagonist, bound saturably and reversibly to rat adrenal membranes. Tritium 1-3 angiotensinogen Rattus norvegicus 57-71 1480133-3 1992 The relative potencies of various angiotensin II-related peptide and nonpeptide antagonists in displacing [3H]L-158,809 binding correlated with their potencies in displacing the binding of 125I-Sar1,Ile8-angiotensin II to adrenal AT1 receptors. Tritium 107-109 angiotensinogen Rattus norvegicus 34-48 1480133-5 1992 The potencies of angiotensin II receptor agonists, but not antagonists, in inhibiting specific [3H]L-158,809 binding were decreased in the presence of guanosine-5"-(beta,gamma-imido)triphosphate. Tritium 96-98 angiotensinogen Rattus norvegicus 17-31 1480133-7 1992 Collectively, the data indicate that [3H]L-158,809 represents a new, potent, nonpeptide, antagonist radioligand suitable for the study of angiotensin II AT1 receptors. Tritium 38-40 angiotensinogen Rattus norvegicus 138-152 1415736-4 1992 ANG II (1 microM) evoked an immediate peak (5-10 s) in total [3H]IPs of 60.5 +/- 18.8% (mean +/- SE) above basal (nonstimulated state) in normal glomeruli, and 88.4 +/- 19.4% in diabetic condition [not significant (NS), n = 8]. Tritium 62-64 angiotensinogen Rattus norvegicus 0-6 1322309-2 1992 As little as 37.5 micrograms of AII injected s.c. over an 80 min period caused immediate reductions in [3H]Ro5-4864 binding. Tritium 104-106 angiotensinogen Rattus norvegicus 32-35 1322309-3 1992 Scatchard analysis revealed that the reduction in [3H]Ro5-4864 binding induced by AII was due to a drop in receptor density or Bmax. Tritium 51-53 angiotensinogen Rattus norvegicus 82-85 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 236-238 angiotensinogen Rattus norvegicus 42-56 1855539-1 1991 In the rat lung [3H]angiotensin II ([3H]AII) recognizes a single class of binding sites with an equilibrium constant (KD) of 2.8 +/- 0.9 nM. Tritium 17-19 angiotensinogen Rattus norvegicus 20-34 1855539-1 1991 In the rat lung [3H]angiotensin II ([3H]AII) recognizes a single class of binding sites with an equilibrium constant (KD) of 2.8 +/- 0.9 nM. Tritium 37-39 angiotensinogen Rattus norvegicus 20-34 1551205-4 1992 Ang II alone and in combination with basic fibroblast growth factor induced a small delayed increase (48-72 hours after treatment) in DNA synthesis and [3H]thymidine labeling indexes without an increase in cell number. Tritium 153-155 angiotensinogen Rattus norvegicus 0-6 1543497-4 1992 It was found that AT II significantly enhanced the [3H]-thymidine incorporation into pituitary tumoral cells in the concentrations of 10(-10) and 10(-8) M. The stimulatory effect disappeared at the concentration of 10(-6) M. The possible involvement of pituitary renin-angiotensin system in pituitary tumorigenesis was discussed. Tritium 52-54 angiotensinogen Rattus norvegicus 18-23 1382167-7 1992 In further studies, angiotensin II (Ang II) was shown to decrease potassium-stimulated [3H] acetylcholine release from slices of rat entorhinal and human temporal cortex, an effect that could be antagonized by the angiotensin receptor antagonist [1-sar,8-thr]Ang II. Tritium 88-90 angiotensinogen Rattus norvegicus 20-34 1382167-7 1992 In further studies, angiotensin II (Ang II) was shown to decrease potassium-stimulated [3H] acetylcholine release from slices of rat entorhinal and human temporal cortex, an effect that could be antagonized by the angiotensin receptor antagonist [1-sar,8-thr]Ang II. Tritium 88-90 angiotensinogen Rattus norvegicus 36-42 1382167-7 1992 In further studies, angiotensin II (Ang II) was shown to decrease potassium-stimulated [3H] acetylcholine release from slices of rat entorhinal and human temporal cortex, an effect that could be antagonized by the angiotensin receptor antagonist [1-sar,8-thr]Ang II. Tritium 88-90 angiotensinogen Rattus norvegicus 259-265 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 236-238 angiotensinogen Rattus norvegicus 58-63 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 256-258 angiotensinogen Rattus norvegicus 42-56 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 256-258 angiotensinogen Rattus norvegicus 58-63 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 256-258 angiotensinogen Rattus norvegicus 42-56 1697379-1 1990 In the present studies we have shown that angiotensin II (AT II), in a concentration-dependent manner in rat tissue (10(-9)-10(-5) M) or at a single concentration in human tissue (10(-6) M), can inhibit potassium-stimulated release of [3H]acetylcholine ( [3H]Ach) from slices of rat entorhinal cortex and human temporal cortex preloaded with [3H]choline for the biochemical analyses. Tritium 256-258 angiotensinogen Rattus norvegicus 58-63 1696651-3 1990 The release of 3H from the perfused rat lung in response to intra-arterial injections of Ang II and other hormones was quantitated. Tritium 15-17 angiotensinogen Rattus norvegicus 89-95 2351436-2 1990 A series of nonpeptide angiotensin II (Ang II) receptor antagonists was evaluated in rat adrenal cortical microsomes for their inhibitory effects on the specific binding of [3H]Ang II, in the isolated rabbit aorta bioassay for their functional antagonism of contractile response to Ang II, and in high renin, renal-hypertensive rats for their intravenous antihypertensive effects, expressed as IC50, pA2, and intravenous ED30, respectively. Tritium 174-176 angiotensinogen Rattus norvegicus 39-45 1696651-6 1990 Analysis of this effluent by thin-layer chromatography indicated that most of the Ang II-induced release of 3H was [3H]adenosine. Tritium 108-110 angiotensinogen Rattus norvegicus 82-88 2351436-2 1990 A series of nonpeptide angiotensin II (Ang II) receptor antagonists was evaluated in rat adrenal cortical microsomes for their inhibitory effects on the specific binding of [3H]Ang II, in the isolated rabbit aorta bioassay for their functional antagonism of contractile response to Ang II, and in high renin, renal-hypertensive rats for their intravenous antihypertensive effects, expressed as IC50, pA2, and intravenous ED30, respectively. Tritium 174-176 angiotensinogen Rattus norvegicus 177-183 2351436-2 1990 A series of nonpeptide angiotensin II (Ang II) receptor antagonists was evaluated in rat adrenal cortical microsomes for their inhibitory effects on the specific binding of [3H]Ang II, in the isolated rabbit aorta bioassay for their functional antagonism of contractile response to Ang II, and in high renin, renal-hypertensive rats for their intravenous antihypertensive effects, expressed as IC50, pA2, and intravenous ED30, respectively. Tritium 174-176 angiotensinogen Rattus norvegicus 177-183 2778716-5 1989 Scatchard analysis of the [3H]AII binding revealed that in the presence of EXP6155 (10(-6) M), the dissociation constant for AII was increased from 1.2 to 3.9 X 10(-9) M, whereas the total number of binding sites remained unchanged, suggesting a competitive nature of antagonism. Tritium 27-29 angiotensinogen Rattus norvegicus 30-33 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 201-204 angiotensinogen Rattus norvegicus 107-121 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 201-204 angiotensinogen Rattus norvegicus 123-129 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 201-203 angiotensinogen Rattus norvegicus 107-121 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 201-203 angiotensinogen Rattus norvegicus 123-129 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 216-218 angiotensinogen Rattus norvegicus 107-121 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 216-218 angiotensinogen Rattus norvegicus 123-129 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 216-218 angiotensinogen Rattus norvegicus 107-121 2322238-1 1990 Incubation of primary neuronal cultures prepared from the hypothalamus and brainstem of neonatal rats with angiotensin II (Ang-II) resulted in a concentration-dependent effect on the incorporation of [3H]-tyrosine ([3H]-Tyr) into [3H]-catecholamines ([3H]-CA). Tritium 216-218 angiotensinogen Rattus norvegicus 123-129 2306237-1 1990 The effects of a long-acting somatostatin analog SMS 201-995 injections on the basal and angiotensin II-stimulated [3H]-thymidine uptake by the rat adrenal glands incubated in vitro were examined. Tritium 116-118 angiotensinogen Rattus norvegicus 89-103 1978694-5 1990 The compounds displace 3H-AII from its specific binding sites in adrenal cortical membranes and smooth muscle cells. Tritium 23-25 angiotensinogen Rattus norvegicus 26-29 1708014-5 1990 Ang II caused a significant but similar increase in cell numbers in both GH and N rat cells (i.e., Ang II caused hyperplasia in all four strains) but [3H]thymidine uptake was significantly greater in GH rat cells. Tritium 151-153 angiotensinogen Rattus norvegicus 0-6 2778716-5 1989 Scatchard analysis of the [3H]AII binding revealed that in the presence of EXP6155 (10(-6) M), the dissociation constant for AII was increased from 1.2 to 3.9 X 10(-9) M, whereas the total number of binding sites remained unchanged, suggesting a competitive nature of antagonism. Tritium 27-29 angiotensinogen Rattus norvegicus 125-128 2549161-0 1989 [3H]angiotensin II binding to basolateral membranes from rat proximal renal tubule: effect of sodium intake and captopril. Tritium 1-3 angiotensinogen Rattus norvegicus 4-18 2504985-8 1989 However, CsA, in a dose dependent manner, inhibited A23187 and angiotensin II induced release of 3H-labelled arachidonic acid from rat mesangial cells. Tritium 97-99 angiotensinogen Rattus norvegicus 63-77 2765877-3 1989 Angiotensin II (10(-9)-10(-5) M) (but not angiotensin I) reduced the potassium-induced release of [3H]acetylcholine in a concentration-related manner to 60% of control levels, but did not effect basal tritium release. Tritium 201-208 angiotensinogen Rattus norvegicus 0-14 2549161-4 1989 A single class of specific high-affinity [3H]angiotensin II-binding site was identified in the basolateral membrane preparation which, after correction of results for tracer degradation, showed equilibrium dissociation constant of 0.23 nmol/l and binding site concentration of 485.8 fmol/mg protein. Tritium 42-44 angiotensinogen Rattus norvegicus 45-59 2549161-5 1989 Binding sites for [3H]angiotensin II were measured in basolateral membranes prepared from rats fed diets with a low, normal or high sodium content. Tritium 19-21 angiotensinogen Rattus norvegicus 22-36 3139662-1 1988 The ability of angiotensin II to down-regulate its receptor was tested on rat hepatocytes in primary culture for 4 h. Angiotensin II treatment decreased [3H]angiotensin II specific binding in a concentration- and time-dependent manner. Tritium 154-156 angiotensinogen Rattus norvegicus 15-29 3139397-2 1988 After preincubation of these cells with 1 microCi [3H]AA, a 20-min perifusion with AII (100 nM), TRH (100 nM), or NT (1 microM) elicited a sharp initial increase in PRL release and [3H]AA efflux, which rapidly subsided (within 6 min) to less elevated levels of PRL release and AA liberation. Tritium 182-184 angiotensinogen Rattus norvegicus 83-86 2844791-2 1988 The angiotensin II receptor of cultured rat hepatocytes was characterized using [3H]angiotensin II as radioligand. Tritium 81-83 angiotensinogen Rattus norvegicus 4-18 2852447-0 1988 Angiotensin II reduces the affinity of [3H]para-aminoclonidine binding sites in membrane preparations from the rat dorsomedial medulla oblongata. Tritium 40-42 angiotensinogen Rattus norvegicus 0-14 3392535-3 1988 Following incubation with 3H-labeled isoleucine, radioactively labeled angiotensinogen with an approximate molecular weight of 25,000 was identified in both glial and neuronal cells. Tritium 26-28 angiotensinogen Rattus norvegicus 71-86 2845165-1 1988 Incubation of [3H] inositol-labeled cultured rat aortic vascular smooth muscle cells with angiotensin II caused the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates. Tritium 15-17 angiotensinogen Rattus norvegicus 90-104 3139662-1 1988 The ability of angiotensin II to down-regulate its receptor was tested on rat hepatocytes in primary culture for 4 h. Angiotensin II treatment decreased [3H]angiotensin II specific binding in a concentration- and time-dependent manner. Tritium 154-156 angiotensinogen Rattus norvegicus 118-132 3139662-1 1988 The ability of angiotensin II to down-regulate its receptor was tested on rat hepatocytes in primary culture for 4 h. Angiotensin II treatment decreased [3H]angiotensin II specific binding in a concentration- and time-dependent manner. Tritium 154-156 angiotensinogen Rattus norvegicus 157-171 3126665-9 1988 ANG II inhibited intracellular [3H]NE uptake in a concentration-dependent manner. Tritium 32-34 angiotensinogen Rattus norvegicus 0-6 3126665-10 1988 At a dose of 1 mM, ANG II inhibited intracellular [3H]NE accumulation by 60%. Tritium 51-53 angiotensinogen Rattus norvegicus 19-25 3126665-12 1988 Thus ANG II appears to prevent [3H]NE accumulation within rat jejunum by inhibiting neuronal uptake. Tritium 32-34 angiotensinogen Rattus norvegicus 5-11 2829820-7 1987 Angiotensin II (100 nM) stimulates IP3 formation from membrane preparations of [3H]inositol-labelled mesangial cells with a half-maximal potency of 1.1 nM. Tritium 80-82 angiotensinogen Rattus norvegicus 0-14 3668538-1 1987 Angiotensin II (ANGII) (3-100 nM) facilitated the potassium-evoked (22.5 mM) release of [3H]-noradrenaline ([3H]NA) from slices of parietal cortex in a concentration-dependent manner, but did not significantly alter the release of [3H]NA evoked in a similar manner from locus coeruleus slices. Tritium 89-91 angiotensinogen Rattus norvegicus 0-14 3668538-1 1987 Angiotensin II (ANGII) (3-100 nM) facilitated the potassium-evoked (22.5 mM) release of [3H]-noradrenaline ([3H]NA) from slices of parietal cortex in a concentration-dependent manner, but did not significantly alter the release of [3H]NA evoked in a similar manner from locus coeruleus slices. Tritium 89-91 angiotensinogen Rattus norvegicus 16-21 3668538-1 1987 Angiotensin II (ANGII) (3-100 nM) facilitated the potassium-evoked (22.5 mM) release of [3H]-noradrenaline ([3H]NA) from slices of parietal cortex in a concentration-dependent manner, but did not significantly alter the release of [3H]NA evoked in a similar manner from locus coeruleus slices. Tritium 109-111 angiotensinogen Rattus norvegicus 0-14 3668538-1 1987 Angiotensin II (ANGII) (3-100 nM) facilitated the potassium-evoked (22.5 mM) release of [3H]-noradrenaline ([3H]NA) from slices of parietal cortex in a concentration-dependent manner, but did not significantly alter the release of [3H]NA evoked in a similar manner from locus coeruleus slices. Tritium 109-111 angiotensinogen Rattus norvegicus 16-21 3668538-7 1987 The mechanism underlying the ANGII facilitation of [3H]NA release from the parietal cortex does not appear to involve either nimodipine-sensitive calcium channels, or, as far as we have been able to determine, the release of calcium from intracellular stores following the breakdown of phosphoinositides. Tritium 52-54 angiotensinogen Rattus norvegicus 29-34 3591934-4 1987 In previous studies, we determined that ANG II (10 nM-1 microM) stimulates increased neuronal [3H]NE uptake by acting at specific receptors. Tritium 95-97 angiotensinogen Rattus norvegicus 40-46 2885358-8 1987 Peak plasma counts (less than 5% of total) of [3H]AII in the blood after intrathecal injection occurred 2 min after the peak changes in sympathetic activity and blood pressure. Tritium 47-49 angiotensinogen Rattus norvegicus 50-53 2885358-9 1987 Counts of [3H]AII in the spinal cord showed that 81% of recovered label was within one segment on either side of the catheter tip. Tritium 11-13 angiotensinogen Rattus norvegicus 14-17 3024736-4 1987 Angiotensin II also decreased the 3H radioactivity of PIP slightly only at 15 s and increased that of phosphatidic acid after 15 s, with no significant effect upon the labelings of phosphatidylinositol (PI), phosphatidylcholine (PC) and phosphatidylethanolamine (PE) within 1 min. Tritium 34-36 angiotensinogen Rattus norvegicus 0-14 3036280-2 1987 Enhanced release of either total 3H or 3H-NE after prelabeling with 3H-NE has been demonstrated to occur from the mesenteric vasculature of SHR after administration of isoproterenol or angiotensin II. Tritium 33-35 angiotensinogen Rattus norvegicus 185-199 3826617-9 1986 Only 30% of unretained [3H]angiotensin II could be identified as intact [3H]angiotensin II on HPLC. Tritium 73-75 angiotensinogen Rattus norvegicus 76-90 3499482-1 1987 Rat PC-12 pheochromocytoma cells respond to stimulation with bradykinin, angiotensin II, and carbachol with an increased formation of labeled inositol phosphates after preincubation of the cells with [3H]inositol. Tritium 201-203 angiotensinogen Rattus norvegicus 73-87 3024031-11 1986 In spirally cut strips angiotensin II increased 3H overflow. Tritium 48-50 angiotensinogen Rattus norvegicus 23-37 3020141-1 1986 The hydrolysis of membrane phosphatidylinositol to yield [3H]labelled inositol phosphates by anterior pituitary cells was stimulated significantly by angiotensin II, TRH and neurotensin over a broad range of concentrations. Tritium 58-60 angiotensinogen Rattus norvegicus 150-164 2997859-1 1985 Angiotensin II receptors have been quantitated in single rat adrenal medullas by incubation of tissue sections with 125I-[Sar1]-AII, autoradiography with exposure to 3H-sensitive Ultrofilm, computerized densitometry and comparison with 125I-labelled standards. Tritium 166-168 angiotensinogen Rattus norvegicus 0-14 3763440-1 1986 Angiotensin II binding sites were localized and quantified in individual brain nuclei from single rats by incubation of tissue sections with 1 nM 125I-[Sar1]-angiotensin II, [3H]-Ultrofilm autoradiography, computerized microdensitometry and comparison with 125I-standards. Tritium 175-177 angiotensinogen Rattus norvegicus 0-14 3014392-1 1986 Angiotensin II binding sites were localized in the rat brain by incubation of sagittal sections with 125I-[Sar1]-angiotensin II, followed by [3H]Ultrofilm autoradiography. Tritium 142-144 angiotensinogen Rattus norvegicus 0-14 3718499-2 1986 Glomerular contraction was assessed by the reduction of extracellular [3H]inulin space of glomerulus, mostly composing of intracapillary space, produced by angiotensin II. Tritium 71-73 angiotensinogen Rattus norvegicus 156-170 3090472-2 1986 When [3H]inositol-prelabelled rat anterior hemipituitaries were incubated with AII (10 microM) for 30 min in the presence of Li+ (10 mM), the production of IP, IP2 and IP3 were increased to 182, 199 and 158% of paired control values. Tritium 6-8 angiotensinogen Rattus norvegicus 79-82 3513605-5 1986 In SD or WKY neuronal co-cultures, ANG II (0.1 nM-10 microM) caused increased [3H]NE uptake during short-term incubations (1-5 min). Tritium 79-81 angiotensinogen Rattus norvegicus 35-41 3513605-8 1986 Construction of saturation curves and kinetic analyses revealed that ANG II caused an increase in the maximal velocity of uptake of neuronal [3H]NE, but the affinity of the transporter for NE was not altered. Tritium 142-144 angiotensinogen Rattus norvegicus 69-75 3513605-9 1986 With longer-term incubations (15-30 min), ANG II caused a reduction in neuronal [3H]NE uptake. Tritium 81-83 angiotensinogen Rattus norvegicus 42-48 3513605-12 1986 Therefore, using neuronal co-cultures, we have identified a previously unseen stimulatory action of ANG II on neuronal [3H]NE uptake, which precedes the already documented inhibitory actions. Tritium 120-122 angiotensinogen Rattus norvegicus 100-106 3005828-6 1986 However, IAP treatment decreased [3H]angiotensin II binding affinity when studies were performed in the absence but not the presence of 5"-guanylylimidodiphosphate (GppNHp). Tritium 34-36 angiotensinogen Rattus norvegicus 37-51 3005828-9 1986 The effects of NaCl on [3H]angiotensin II binding were also tested but were not typical of other receptors which couple to Ni. Tritium 24-26 angiotensinogen Rattus norvegicus 27-41 6747630-4 1984 Analysis of radioimmunoassay data revealed an increase in the amount of tritium-labeled angiotensin II in the crude extract of the brain cells during the first 24 h in culture. Tritium 72-79 angiotensinogen Rattus norvegicus 88-102 6084790-1 1984 This study investigated the ability of angiotensin II (Ang II) to facilitate the stimulation-induced release of [3H]norepinephrine [( 3H]NE) from two cardiovascular regulatory areas in normal and sodium-restricted rats. Tritium 113-115 angiotensinogen Rattus norvegicus 39-53 6084790-1 1984 This study investigated the ability of angiotensin II (Ang II) to facilitate the stimulation-induced release of [3H]norepinephrine [( 3H]NE) from two cardiovascular regulatory areas in normal and sodium-restricted rats. Tritium 113-115 angiotensinogen Rattus norvegicus 55-61 6084790-2 1984 Ang II (10(-7) M) facilitated the field-stimulation-induced release of [3H]NE from the A2 area of the nucleus tractus solitarius but not from the anterior hypothalamus of Sprague-Dawley and Wistar rats. Tritium 72-74 angiotensinogen Rattus norvegicus 0-6 6084790-3 1984 Placement of rats on a sodium-restricted diet abolished the facilitation of [3H]NE release due to Ang II. Tritium 77-79 angiotensinogen Rattus norvegicus 98-104 6084790-6 1984 Seven-day intravenous Ang II infusions blocked the facilitory effect of Ang II on [3H]NE release in a manner similar to that seen with sodium restriction. Tritium 83-85 angiotensinogen Rattus norvegicus 22-28 6084790-6 1984 Seven-day intravenous Ang II infusions blocked the facilitory effect of Ang II on [3H]NE release in a manner similar to that seen with sodium restriction. Tritium 83-85 angiotensinogen Rattus norvegicus 72-78 6084790-7 1984 These results suggest that low sodium diets may alter the facilitation of [3H]NE release by Ang II by interactions with the renin-angiotensin system. Tritium 75-77 angiotensinogen Rattus norvegicus 92-98 6747630-3 1984 The time-dependent incorporation of [3H]proline into newly synthesized angiotensin II-like peptide was measured by radioimmunoassay using specific angiotensin II antisera. Tritium 36-39 angiotensinogen Rattus norvegicus 71-85 6747630-3 1984 The time-dependent incorporation of [3H]proline into newly synthesized angiotensin II-like peptide was measured by radioimmunoassay using specific angiotensin II antisera. Tritium 36-39 angiotensinogen Rattus norvegicus 147-161 6331586-6 1984 [3H]AI and [3H]AII yielded the same [3H]metabolites corresponding to two peaks alpha and beta. Tritium 12-14 angiotensinogen Rattus norvegicus 15-18 6331586-6 1984 [3H]AI and [3H]AII yielded the same [3H]metabolites corresponding to two peaks alpha and beta. Tritium 12-14 angiotensinogen Rattus norvegicus 15-18 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 160-162 angiotensinogen Rattus norvegicus 53-56 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 160-162 angiotensinogen Rattus norvegicus 87-90 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 160-162 angiotensinogen Rattus norvegicus 87-90 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 173-175 angiotensinogen Rattus norvegicus 53-56 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 173-175 angiotensinogen Rattus norvegicus 87-90 6331586-7 1984 Nevertheless, by adding an excess of unlabeled Ileu5-AII, which competitively inhibits AII-angiotensinase activity, it was possible to detect the formation of [3H]AII from [3H]AI. Tritium 173-175 angiotensinogen Rattus norvegicus 87-90 6324207-10 1984 The presence of [3H]captopril binding is consistent with an ACE-mediated production of angiotensin II in some brain regions. Tritium 17-19 angiotensinogen Rattus norvegicus 87-101 6100309-11 1984 Authentic 3H-AII was not detected, but two smaller peptides appeared (peak alpha et beta). Tritium 10-12 angiotensinogen Rattus norvegicus 13-16 6100309-12 1984 The same peaks appeared when rat brain was incubated with 3H-AII. Tritium 58-60 angiotensinogen Rattus norvegicus 61-64 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 33-35 angiotensinogen Rattus norvegicus 36-39 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 33-35 angiotensinogen Rattus norvegicus 75-78 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 33-35 angiotensinogen Rattus norvegicus 75-78 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 55-57 angiotensinogen Rattus norvegicus 36-39 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 55-57 angiotensinogen Rattus norvegicus 75-78 6100309-13 1984 We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C). Tritium 55-57 angiotensinogen Rattus norvegicus 75-78 6658140-2 1983 The total 3H outflow of radioactivity was higher in AII exposed tissues than in nephrectomized ones of both organs. Tritium 10-12 angiotensinogen Rattus norvegicus 52-55 6498633-1 1984 125I-labelled angiotensin II (AII) and [3H]AII showed specific binding to rat mesenteric artery microsomes. Tritium 40-42 angiotensinogen Rattus norvegicus 43-46 6498633-3 1984 [3H]AII was not degraded by the microsomes but 125I-labelled AII was degraded. Tritium 1-3 angiotensinogen Rattus norvegicus 4-7 6498633-3 1984 [3H]AII was not degraded by the microsomes but 125I-labelled AII was degraded. Tritium 1-3 angiotensinogen Rattus norvegicus 61-64 6498633-5 1984 Chromatography of unlabelled AII or [3H]AII gave the same Rf value as 125I-labelled AII, but unlabelled AIII moved with Rf = 0.55-0.60. Tritium 37-39 angiotensinogen Rattus norvegicus 40-43 6498633-5 1984 Chromatography of unlabelled AII or [3H]AII gave the same Rf value as 125I-labelled AII, but unlabelled AIII moved with Rf = 0.55-0.60. Tritium 37-39 angiotensinogen Rattus norvegicus 40-43 6188430-3 1982 Intraventricularly infused [3H] NE uptake increased in hypothalamus and medulla oblongata of nephrectomized animals in cytoplasmatic compartment as in granular stores, while it decreased in hypothalamus of AII-infused animals. Tritium 28-30 angiotensinogen Rattus norvegicus 206-209 6828210-4 1983 Incubation of cultures with Captopril, an inhibitor of the converting enzyme, resulted in a significant inhibition of [3H]-valine incorporation into immunoreactive [3H]-angiotensin II. Tritium 119-121 angiotensinogen Rattus norvegicus 169-183 6828210-4 1983 Incubation of cultures with Captopril, an inhibitor of the converting enzyme, resulted in a significant inhibition of [3H]-valine incorporation into immunoreactive [3H]-angiotensin II. Tritium 165-167 angiotensinogen Rattus norvegicus 169-183 6188430-4 1982 [3H] NE metabolites radioactivity decreased in nephrectomized animals if they are compared with AII-infused ones. Tritium 1-3 angiotensinogen Rattus norvegicus 96-99 6188430-6 1982 The study of the ratio granular/cytoplasmatic [3H] NE and metabolites radioactivity shows that AII probably acts on cellular membrane uptake of NE. Tritium 47-49 angiotensinogen Rattus norvegicus 95-98 6188430-8 1982 The effects of AII and nephrectomy on [3H] NE uptake can explain the inverse relationship between circulating AII levels and NE content in the central nervous system (CNS). Tritium 39-41 angiotensinogen Rattus norvegicus 15-18 6188430-8 1982 The effects of AII and nephrectomy on [3H] NE uptake can explain the inverse relationship between circulating AII levels and NE content in the central nervous system (CNS). Tritium 39-41 angiotensinogen Rattus norvegicus 110-113 31974621-6 2020 The morphology and surface area of the H9c2 cells, the expression of hypertrophic markers and TRPC channel-related proteins and the [3H] leucine incorporation rate were detected in the Ang II-treated H9c2 cells following treatment with the TRPC channel inhibitor SKF-96365. Tritium 133-135 angiotensinogen Rattus norvegicus 185-191 179329-1 1976 125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Tritium 52-54 angiotensinogen Rattus norvegicus 55-69 179329-1 1976 125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Tritium 72-74 angiotensinogen Rattus norvegicus 13-27 179329-1 1976 125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Tritium 72-74 angiotensinogen Rattus norvegicus 55-69 210990-2 1975 3H-labelled angiotensin II specfically binds to plasma membranes of rat uterine smooth muscle cells. Tritium 0-2 angiotensinogen Rattus norvegicus 12-26 210990-9 1975 Angiotensin II infusion in nephrectomized rats reduced the concentration of 3H-labelled angiotensin-binding sites. Tritium 76-78 angiotensinogen Rattus norvegicus 0-14 33334620-8 2021 Consequently, inhibiting PKCe, PKD and ERK5 by siRNA significantly attenuated Ang II-induced MEF2D activation, ANP and BNP mRNA expression, and [3H]-Leu incorporation. Tritium 145-147 angiotensinogen Rattus norvegicus 78-84 7308897-3 1981 The metabolic ability of [3H]-AII in each nephron segment, was also studied. Tritium 26-28 angiotensinogen Rattus norvegicus 30-33 7308897-8 1981 From the investigation of the metabolic ability of [3H]-AII in each nephron segment, AII was found to be highly metabolized both in the glomerulus and in the proximal tubule, especially in the pars recta. Tritium 52-54 angiotensinogen Rattus norvegicus 56-59 7308897-8 1981 From the investigation of the metabolic ability of [3H]-AII in each nephron segment, AII was found to be highly metabolized both in the glomerulus and in the proximal tubule, especially in the pars recta. Tritium 52-54 angiotensinogen Rattus norvegicus 85-88 6245942-1 1980 The angiotensin II receptor in the rabbit, rat and human adrenal gland and that in the rabbit and rat aorta were studied by using [3H]-angiotensin II ([3H]-AII). Tritium 131-133 angiotensinogen Rattus norvegicus 135-149 1071653-8 1976 During intravenous infusions of 3H-labelled AII at pressor doses small amounts of radioactivity were found in cerebrospinal fluid perfusate. Tritium 32-34 angiotensinogen Rattus norvegicus 44-47 186277-1 1976 3H-labelled angiotensin II binding to receptor sites was studied in plasma membranes isolated from myometrial homogenates of uterine horns. Tritium 0-2 angiotensinogen Rattus norvegicus 12-26 193669-1 1976 3H-labelled angiotensin II binding to receptor sites was studied in plasma membranes isolated from myometrial homogenates of uterine horns. Tritium 0-2 angiotensinogen Rattus norvegicus 12-26 31974621-9 2020 The fluorescence intensity of alpha-actinin, the expression of hypertrophic markers and TRPC-related proteins, the [3H] leucine incorporation rate and the intracellular Ca2+ concentration were all markedly increased in the Ang II-treated H9c2 cells but decreased following SKF-96365 treatment. Tritium 116-118 angiotensinogen Rattus norvegicus 223-229 25362207-8 2015 Angiotensin II-stimulated incorporation of 3[H]leucine in cardiac myocytes and 3[H]proline in cardiac fibroblast was used to evaluate hypertrophy and fibrosis, respectively. Tritium 43-47 angiotensinogen Rattus norvegicus 0-14 25739102-9 2015 The expression of hypertrophic markers and p-ERK2, the cell surface area and the [3H]Leucine incorporation rate were all significantly increased in the AngII-treated cells. Tritium 82-84 angiotensinogen Rattus norvegicus 152-157 24224084-7 2013 At doses that lowered body weight, AngII significantly increased ISBAT [3H]NIS binding density. Tritium 72-74 angiotensinogen Rattus norvegicus 35-40 25082750-9 2014 Addition of low concentrations of PAR agonists to cardiomyocytes treated with ET-1 or Ang II suppressed [(3)H]phenylalanine incorporation induced by the hypertrophic stimuli. Tritium 106-110 angiotensinogen Rattus norvegicus 86-92 24039778-5 2013 In vitro, quercetin also significantly attenuated Ang II-induced H9C2 cells hypertrophy, as indicated by its concentration dependent inhibitory effects on [3H]leucine incorporation into H9C2 cells (64% reduction) and by the reduced hypertrophic surface area in H9C2 cells compared with the Ang II group (P<0.01, vs. Ang II group). Tritium 156-158 angiotensinogen Rattus norvegicus 50-56 23842595-5 2013 We found that TMP significantly inhibited the Ang II-induced hypertrophic growth of neonatal cardiomyocytes, as evidenced by the decrease in [3H]leucine incorporation and beta-myosin heavy chain (beta-MHC) mRNA expression. Tritium 142-144 angiotensinogen Rattus norvegicus 46-52 20927110-5 2010 Mechanical stretch attenuated AngII-induced phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, ERK kinase (MEK) and EGF receptor; it also attenuated [3H] thymidine incorporation and cell proliferation in VSMC of WKY. Tritium 167-169 angiotensinogen Rattus norvegicus 30-35 19293600-6 2009 ANG II effects on [(3)H]-DA uptake were able to modify Na(+),K(+)-ATPase activity in carbidopa-treated rats. Tritium 18-23 angiotensinogen Rattus norvegicus 0-6 20845786-7 2010 RESULTS: High glucose (30 mmol/L) and Ang II (10(-7) mol/L) induced hypertrophy of renal proximal tubular epithelial cells result in, cell size, 3H-leucine incorporation and cellular protein content increased significantly. Tritium 145-147 angiotensinogen Rattus norvegicus 38-44 18971538-8 2008 In cultured VSMCs, [3H]TdR and [3H]proline incorporation stimulated by angiotensin II was inhibited by incubation with NaHS. Tritium 20-22 angiotensinogen Rattus norvegicus 71-85 18971538-8 2008 In cultured VSMCs, [3H]TdR and [3H]proline incorporation stimulated by angiotensin II was inhibited by incubation with NaHS. Tritium 32-34 angiotensinogen Rattus norvegicus 71-85