PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 14709140-7 2004 This could indicate a defined biological function of the CNP/GC-B/cGMP axis in gestation e.g. antagonizing vasoconstrictive peptides like angiotensin II. Cyclic GMP 66-70 angiotensinogen Homo sapiens 138-152 15158138-5 2004 Secondly, ANG stimulates the release of nitric oxide (NO)/cGMP via AT(2) receptor activation, as described in the aorta, heart, and kidney. Cyclic GMP 58-62 angiotensinogen Homo sapiens 10-13 21143283-13 1996 It is concluded that there is a receptor-mediated action of ANF on proximal tubule reabsorption acting via elevation of cGMP to inhibit AngII-stimulated sodium transport. Cyclic GMP 120-124 angiotensinogen Homo sapiens 136-141 12135744-3 2002 AT2 activation by angiotensin II resulted in reduction of cGMP levels in oocytes and this reduction was further enhanced by C-terminal deletion, implying that the C-terminus may have a negative effect on the AT2-mediated cGMP reduction. Cyclic GMP 58-62 angiotensinogen Homo sapiens 18-32 12135744-3 2002 AT2 activation by angiotensin II resulted in reduction of cGMP levels in oocytes and this reduction was further enhanced by C-terminal deletion, implying that the C-terminus may have a negative effect on the AT2-mediated cGMP reduction. Cyclic GMP 221-225 angiotensinogen Homo sapiens 18-32 10691781-7 2000 In the gastrointestinal tract, physiological quantities of ANG II stimulate the AT2 receptor releasing NO and cGMP leading to increased sodium and water absorption. Cyclic GMP 110-114 angiotensinogen Homo sapiens 59-65 9453327-14 1998 The effects of ANG II and of losartan plus ANG II on aortic cGMP content were both blocked by cotreatment with the AT2 receptor antagonist PD 123319. Cyclic GMP 60-64 angiotensinogen Homo sapiens 15-21 9453327-14 1998 The effects of ANG II and of losartan plus ANG II on aortic cGMP content were both blocked by cotreatment with the AT2 receptor antagonist PD 123319. Cyclic GMP 60-64 angiotensinogen Homo sapiens 43-49 9453327-15 1998 Icatibant and L-NAME abolished the effects of ANG II on aortic cGMP. Cyclic GMP 63-67 angiotensinogen Homo sapiens 46-52 8831498-6 1996 In contrast, Ang II directly antagonized NO donor- and cGMP analogue-induced apoptosis via activation of the type I Ang II receptor. Cyclic GMP 55-59 angiotensinogen Homo sapiens 13-19 8831498-6 1996 In contrast, Ang II directly antagonized NO donor- and cGMP analogue-induced apoptosis via activation of the type I Ang II receptor. Cyclic GMP 55-59 angiotensinogen Homo sapiens 116-122 10915802-2 2000 The vasoactive peptides vasopressin, angiotensin II, and endothelin inhibit natriuretic peptide-dependent cGMP elevations by activating protein kinase C (PKC). Cyclic GMP 106-110 angiotensinogen Homo sapiens 37-51 10981149-7 2000 In addition, it is now apparent that the therapeutic reduction in BP with AT1 receptor blockade (eg, losartan, valsartan, candesartan) is mediated by ANG II stimulation of the AT2 receptor, leading to increased levels of BK, NO, and cGMP. Cyclic GMP 233-237 angiotensinogen Homo sapiens 150-156 10754364-16 1999 The significant elevation in cGMP and NO levels in plasma and urine implies a maintained vasodilatory action that may at least partly compensate the vasoconstrictor effects of angiotensin II. Cyclic GMP 29-33 angiotensinogen Homo sapiens 176-190 9751482-4 1998 Type A natriuretic peptide and deta nonoate attenuated angiotensin II-stimulated aldosterone production over the same concentration range that stimulated cGMP production. Cyclic GMP 154-158 angiotensinogen Homo sapiens 55-69 9453327-13 1998 Aortic cGMP content was significantly increased by ANG II, losartan, losartan plus ANG II, and minoxidil plus ANG II by 60%, 45%, 68%, and 52%, respectively (P<.05). Cyclic GMP 7-11 angiotensinogen Homo sapiens 51-57 9453327-13 1998 Aortic cGMP content was significantly increased by ANG II, losartan, losartan plus ANG II, and minoxidil plus ANG II by 60%, 45%, 68%, and 52%, respectively (P<.05). Cyclic GMP 7-11 angiotensinogen Homo sapiens 83-89 9453327-13 1998 Aortic cGMP content was significantly increased by ANG II, losartan, losartan plus ANG II, and minoxidil plus ANG II by 60%, 45%, 68%, and 52%, respectively (P<.05). Cyclic GMP 7-11 angiotensinogen Homo sapiens 83-89 8393287-6 1993 ANP was found to significantly enhance macrophage guanosine 3",5"-cyclic monophosphate (cGMP) levels compared with control cells, and this effect was antagonized by angiotensin II. Cyclic GMP 88-92 angiotensinogen Homo sapiens 165-179 8993849-13 1996 It is concluded that there is a receptor-mediated action of ANF on proximal tubule reabsorption acting via elevation of cGMP to inhibit AngII-stimulated sodium transport. Cyclic GMP 120-124 angiotensinogen Homo sapiens 136-141 8231024-3 1993 Ang II action in mesangial cells was evaluated by measuring the ability of Ang II to inhibit ANP-induced cGMP accumulation through both activating phosphodiesterase (initial phase) and inhibiting guanylate cyclase (maintenance phase). Cyclic GMP 105-109 angiotensinogen Homo sapiens 0-6 8231024-3 1993 Ang II action in mesangial cells was evaluated by measuring the ability of Ang II to inhibit ANP-induced cGMP accumulation through both activating phosphodiesterase (initial phase) and inhibiting guanylate cyclase (maintenance phase). Cyclic GMP 105-109 angiotensinogen Homo sapiens 75-81 1719265-0 1991 Dual mechanism of angiotensin II inhibits ANP-induced mesangial cGMP accumulation. Cyclic GMP 64-68 angiotensinogen Homo sapiens 18-32 1313393-0 1992 C-type natriuretic peptide inhibits thrombin- and angiotensin II-stimulated endothelin release via cyclic guanosine 3",5"-monophosphate. Cyclic GMP 99-135 angiotensinogen Homo sapiens 50-64 1313393-9 1992 Our results suggest that CNP probably inhibits the endothelin-1 secretion stimulated by thrombin and Ang II through a cyclic GMP-dependent process. Cyclic GMP 118-128 angiotensinogen Homo sapiens 101-107 1645748-9 1991 These findings suggest that human ANP and BNP inhibit endothelin-1 secretion stimulated by ANGII and thrombin in these cells through a cyclic GMP-dependent process. Cyclic GMP 135-145 angiotensinogen Homo sapiens 91-96 2853737-3 1988 The down-regulation provoked by Ang II was associated with an enhancement of ANF-stimulated cyclic (c) GMP formation and was confined to the non-guanylate cyclase-coupled ANF receptor subtype. Cyclic GMP 92-106 angiotensinogen Homo sapiens 32-38 176170-0 1976 Effect of angiotensin II on cyclic guanosine monophosphate and cyclic adenosine monophosphate in human plasma. Cyclic GMP 28-58 angiotensinogen Homo sapiens 10-24 2845821-7 1988 Guanosine 3",5"-cyclic monophosphate (cGMP) levels in the aorta increased 15 s after ANG II application. Cyclic GMP 0-36 angiotensinogen Homo sapiens 85-91 2845821-7 1988 Guanosine 3",5"-cyclic monophosphate (cGMP) levels in the aorta increased 15 s after ANG II application. Cyclic GMP 38-42 angiotensinogen Homo sapiens 85-91 2845821-9 1988 These results suggest that ANG II-induced relaxation of fowl aortas involves 1) an endothelium-dependent mechanism and 2) cGMP but not arachidonic acid metabolites. Cyclic GMP 122-126 angiotensinogen Homo sapiens 27-33 2440311-2 1987 Angiotensin II (ANG II) markedly decreased the accumulation of cGMP that was evoked by ANF. Cyclic GMP 63-67 angiotensinogen Homo sapiens 0-14 2440311-2 1987 Angiotensin II (ANG II) markedly decreased the accumulation of cGMP that was evoked by ANF. Cyclic GMP 63-67 angiotensinogen Homo sapiens 16-22 2440311-3 1987 Arginine vasopressin and ATP, which evoke transient increases in free Ca2+ similarly to ANG II, also inhibited cGMP accumulation. Cyclic GMP 111-115 angiotensinogen Homo sapiens 88-94 2440311-5 1987 The cyclic nucleotide phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, prevented ANG II from inhibiting ANF-evoked cGMP accumulation. Cyclic GMP 124-128 angiotensinogen Homo sapiens 90-96 2440311-6 1987 ANG II also inhibited cGMP accumulation induced by nitroprusside, a compound that activates cytosolic guanylate cyclase. Cyclic GMP 22-26 angiotensinogen Homo sapiens 0-6 2440311-7 1987 These findings support the hypothesis that ANG II decreases cGMP accumulation by stimulating cGMP hydrolysis, apparently via a Ca2+-activated cGMP phosphodiesterase. Cyclic GMP 60-64 angiotensinogen Homo sapiens 43-49 2440311-7 1987 These findings support the hypothesis that ANG II decreases cGMP accumulation by stimulating cGMP hydrolysis, apparently via a Ca2+-activated cGMP phosphodiesterase. Cyclic GMP 93-97 angiotensinogen Homo sapiens 43-49 18619489-7 2008 The intracellular effects of Ang II are influenced by nitric oxide (NO)/cGMP-dependent cross talk and are mediated by the release of autocrine factors, such as transforming growth factor (TGF)-beta1 and interleukin (IL)-6. Cyclic GMP 72-76 angiotensinogen Homo sapiens 29-35 32152395-4 2020 ANG II significantly decreased NPRA mRNA and protein levels and cGMP accumulation in cultured mesangial cells and attenuated ANP-mediated relaxation of aortic rings ex vivo. Cyclic GMP 64-68 angiotensinogen Homo sapiens 0-6 28428931-7 2017 In rodents and rabbits, the effect on proximal tubule NBCe1 is biphasic; at low concentration, angiotensin II stimulates NBCe1 via PKC/cAMP/ERK, whereas at high concentration, it inhibits NBCe1 via NO/cGMP/cGKII. Cyclic GMP 201-205 angiotensinogen Homo sapiens 95-109 28428931-8 2017 In contrast, in human proximal tubule, angiotensin II has a dose-dependent monophasic stimulatory effect via NO/cGMP/ERK. Cyclic GMP 112-116 angiotensinogen Homo sapiens 39-53 29181400-6 2017 Notably, our recent functional analysis of isolated proximal tubules demonstrated that Ang II dose-dependently stimulated human proximal tubular Na+ transport through the NO/guanosine 3",5"-cyclic monophosphate (cGMP) pathway, confirming the human-specific regulation of proximal tubular transport via NO and Ang II. Cyclic GMP 174-210 angiotensinogen Homo sapiens 87-93 29181400-6 2017 Notably, our recent functional analysis of isolated proximal tubules demonstrated that Ang II dose-dependently stimulated human proximal tubular Na+ transport through the NO/guanosine 3",5"-cyclic monophosphate (cGMP) pathway, confirming the human-specific regulation of proximal tubular transport via NO and Ang II. Cyclic GMP 212-216 angiotensinogen Homo sapiens 87-93 20489655-5 2010 The experimental results showed that the cytotoxic effects of Ang II on human umbilical vein endothelial cells were significantly ameliorated by atorvastatin pretreatment (LDH tests, MTT assay, and propdium iodide (PI)/Annexin V-stating analysis), and atorvastatin treatment simultaneously enhanced expression of endothelial nitric oxide synthase and yielded of nitric oxide (NO) and cyclic guanosine monophosphate, but both effects were attenuated by the B2Rs antagonist HOE-140. Cyclic GMP 384-414 angiotensinogen Homo sapiens 62-68 20299462-7 2010 Ang II increased cGMP accumulation by 4.9 +/- 1.3 fmol/microg (p < 0.01). Cyclic GMP 17-21 angiotensinogen Homo sapiens 0-6 27092079-6 2016 Ang II-induced protein synthesis was attenuated by pre-treatment with APN, NO donor S-nitroso-N-acetylpenicillamine (SNAP), or cGMP. Cyclic GMP 127-131 angiotensinogen Homo sapiens 0-6 24511122-0 2014 Angiotensin II dose-dependently stimulates human renal proximal tubule transport by the nitric oxide/guanosine 3",5"-cyclic monophosphate pathway. Cyclic GMP 101-137 angiotensinogen Homo sapiens 0-14 24511122-7 2014 Conversely, in human PTs, the NO/cGMP pathway mediated the stimulatory effect of Ang II by phosphorylating ERK independently of cGKII. Cyclic GMP 33-37 angiotensinogen Homo sapiens 81-87 24511122-8 2014 These contrasting responses to the NO/cGMP pathway may largely explain the different modes of PT transport regulation by Ang II, and the unopposed marked stimulation of PT transport by high intrarenal concentrations of Ang II may be an important factor in the pathogenesis of human hypertension. Cyclic GMP 38-42 angiotensinogen Homo sapiens 121-127 22027011-9 2011 Under physiological conditions, activation of a cGMP-dependent pathway moderates the Ca(2+)(i)-enhancing action of hypertrophic factors such as angiotensin II. Cyclic GMP 48-52 angiotensinogen Homo sapiens 144-158 18713751-8 2008 Finally, treatment of mice with angiotensin II (300 ng/kg/min during 7 days) resulted in enhanced pulmonary mRNA expression of spliced GC-A, which was concomitant to diminished GC-A/cGMP responses to ANP. Cyclic GMP 182-186 angiotensinogen Homo sapiens 32-46 17229984-7 2006 Ang II suppressed the ANP-dependent cGMP synthesis whereas SNAP-dependent cGMP production remained unaffected. Cyclic GMP 36-40 angiotensinogen Homo sapiens 0-6 17229984-11 2006 We conclude that cGMP synthesis in cultured podocytes is modulated by angiotensin II and that two adversely acting receptors, AT1 and AT2 are involved in this effect. Cyclic GMP 17-21 angiotensinogen Homo sapiens 70-84