PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22834797-4 2012 Consistent with this observation, chronic treatment of cardiomyocytes with G-protein coupled receptor agonists endothelin-1, angiotensin II, or phenylephrine, agents that are known to produce intracellular IP3, leads to cardiomyopathy and heart failure. Inositol 1,4,5-Trisphosphate 206-209 angiotensinogen Homo sapiens 125-139 20201888-4 2010 The involvement of 1,4,5-IP3-dependent intracellular Ca2+ release in AT-I-induced effects was supported by these findings: the effects of AT-II were blocked by 2-aminoethoxyphenyl borate (2-APB, a 1,4,5-IP3 receptor blocker) and U73122 (a phosopholipase C blocker); and hESC-CM express AT-II type 1 and IP3 type I and II receptors as determined by fluorescence immunostaining. Inositol 1,4,5-Trisphosphate 19-28 angiotensinogen Homo sapiens 138-143 20584908-0 2010 Activation of Na+/H+ exchanger NHE3 by angiotensin II is mediated by inositol 1,4,5-triphosphate (IP3) receptor-binding protein released with IP3 (IRBIT) and Ca2+/calmodulin-dependent protein kinase II. Inositol 1,4,5-Trisphosphate 98-101 angiotensinogen Homo sapiens 39-53 20201888-4 2010 The involvement of 1,4,5-IP3-dependent intracellular Ca2+ release in AT-I-induced effects was supported by these findings: the effects of AT-II were blocked by 2-aminoethoxyphenyl borate (2-APB, a 1,4,5-IP3 receptor blocker) and U73122 (a phosopholipase C blocker); and hESC-CM express AT-II type 1 and IP3 type I and II receptors as determined by fluorescence immunostaining. Inositol 1,4,5-Trisphosphate 19-28 angiotensinogen Homo sapiens 286-291 21547002-8 2009 In vascular smooth muscle, vasoconstrictors such as angiotensin II, endothelin-1 and norepinephrine stimulate contraction by increasing inositol trisphosphate (IP(3)), calcium, DG and PKC activity. Inositol 1,4,5-Trisphosphate 160-165 angiotensinogen Homo sapiens 52-66 18948082-1 2008 The heterotrimeric guanine nucleotide-binding protein Galphaq transduces signals from heptahelical transmembrane receptors (e.g., alpha(1)-adrenergic, endothelin 1A, and angiotensin II) to stimulate generation of inositol-1,4,5-trisphosphate and diacylglycerol. Inositol 1,4,5-Trisphosphate 213-241 angiotensinogen Homo sapiens 170-184 18562632-2 2008 ANG II stimulation was simulated by doubling maximal inositol trisphosphate (IP3) production and imposing a 90% blockade of K+ channels. Inositol 1,4,5-Trisphosphate 77-80 angiotensinogen Homo sapiens 0-6 17299068-8 2007 BMC also attenuated the AII-induced increase in cytoplasmic calcium, partially through an inhibition of cytoplasmic inositol 1,4,5 triphosphate production. Inositol 1,4,5-Trisphosphate 116-143 angiotensinogen Homo sapiens 24-27 18171914-13 2008 Furthermore, the D4R agonist enhanced the AII-stimulated elevation of intracellular IP(3) and [Ca(2+)](i). Inositol 1,4,5-Trisphosphate 84-89 angiotensinogen Homo sapiens 42-45 15044681-4 2004 ANG II, bound to AT(1) receptors, acts through the inositol 1,4,5-trisphosphate (IP(3))-Ca(2+)/calmodulin system. Inositol 1,4,5-Trisphosphate 51-79 angiotensinogen Homo sapiens 0-6 15044681-4 2004 ANG II, bound to AT(1) receptors, acts through the inositol 1,4,5-trisphosphate (IP(3))-Ca(2+)/calmodulin system. Inositol 1,4,5-Trisphosphate 81-87 angiotensinogen Homo sapiens 0-6 14523024-7 2003 Deletion mutation analysis showed that GIT1(SHD) is required for AngII- and EGF-mediated PLCgamma activation (measured by phosphorylation of Tyr783 and inositol 1,4,5-trisphosphate formation). Inositol 1,4,5-Trisphosphate 152-180 angiotensinogen Homo sapiens 65-70 14612458-10 2004 However, another physiological agent linked to phospholipase C and inositol 1,4,5-trisphosphate cascade, angiotensin II, produced a striking Ca2+ transient. Inositol 1,4,5-Trisphosphate 67-95 angiotensinogen Homo sapiens 105-119 14660489-8 2004 Nevertheless, at high [Cl-], the peak increase of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] induced by ANG II was approximately sixfold that at low [Cl-]. Inositol 1,4,5-Trisphosphate 50-78 angiotensinogen Homo sapiens 105-111 14660489-8 2004 Nevertheless, at high [Cl-], the peak increase of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] induced by ANG II was approximately sixfold that at low [Cl-]. Inositol 1,4,5-Trisphosphate 80-92 angiotensinogen Homo sapiens 105-111 10467229-5 1999 This receptor is coupled to the G-protein Gq, which mediates AngII-induced inositol triphosphate (IP3) formation. Inositol 1,4,5-Trisphosphate 98-101 angiotensinogen Homo sapiens 61-66 12374782-7 2002 Our data indicate that ANG II acting in the NTS depresses the baroreflex via a Gq protein-mediated activation of phospholipase C, which through 1,4,5-inositol triphosphate causes release of calcium from the IP3-sensitive intracellular stores and calcium-calmodulin formation. Inositol 1,4,5-Trisphosphate 207-210 angiotensinogen Homo sapiens 23-29 11433227-13 2001 In summary, ANG II increases extracellular/intracellular calcium dependent bidirectional Ca2(+) transport in GECs, inhibits BK induced release of Ca2(+) from IP(3) sensitive stores, and, in addition, reduces refilling of endoplasmic reticulum [Ca2(+)] depleted by repeated BK stimulation. Inositol 1,4,5-Trisphosphate 158-163 angiotensinogen Homo sapiens 12-18 11134246-0 2001 Iloprost inhibits inositol-1,4,5-trisphosphate-mediated calcium mobilization stimulated by angiotensin II in cultured preglomerular vascular smooth muscle cells. Inositol 1,4,5-Trisphosphate 18-46 angiotensinogen Homo sapiens 91-105 21331728-4 2001 One of the earliest measurable events resulting from Ang II stimulation of vascular smooth muscle cells, is a rapid, phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate, to produce two second messengers, 1,2 diacylglycerol and inositol 1,4,5-trisphosphate (IP(3)) (7,8). Inositol 1,4,5-Trisphosphate 258-286 angiotensinogen Homo sapiens 53-59 21331728-4 2001 One of the earliest measurable events resulting from Ang II stimulation of vascular smooth muscle cells, is a rapid, phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate, to produce two second messengers, 1,2 diacylglycerol and inositol 1,4,5-trisphosphate (IP(3)) (7,8). Inositol 1,4,5-Trisphosphate 288-293 angiotensinogen Homo sapiens 53-59 10467229-8 1999 This increase in AT1 binding resulted in enhanced AngII-stimulated IP3 formation. Inositol 1,4,5-Trisphosphate 67-70 angiotensinogen Homo sapiens 50-55 10467229-11 1999 These results indicate that GR activation, and the subsequent increases in AT1 binding and in AngII-stimulated IP3 formation, may represent a cellular mechanism underlying the synergy between adrenal steroids and AngII. Inositol 1,4,5-Trisphosphate 111-114 angiotensinogen Homo sapiens 94-99 10467229-11 1999 These results indicate that GR activation, and the subsequent increases in AT1 binding and in AngII-stimulated IP3 formation, may represent a cellular mechanism underlying the synergy between adrenal steroids and AngII. Inositol 1,4,5-Trisphosphate 111-114 angiotensinogen Homo sapiens 213-218 9595533-7 1998 Ang II- or Epi-induced IP3 production in HUVECs incubated with PIH serum was increased but not significantly compared to that with other sera. Inositol 1,4,5-Trisphosphate 23-26 angiotensinogen Homo sapiens 0-6 10361980-1 1999 Previous studies have shown that while vasopressin and angiotensin II are markedly more effective than norepinephrine and prostaglandin F2alpha in eliciting an acute elevation of inositol 1,4,5-trisphosphate (IP3), norepinephrine and prostaglandin F2alpha produce larger enhancement of DNA synthesis. Inositol 1,4,5-Trisphosphate 179-207 angiotensinogen Homo sapiens 55-69 10361980-1 1999 Previous studies have shown that while vasopressin and angiotensin II are markedly more effective than norepinephrine and prostaglandin F2alpha in eliciting an acute elevation of inositol 1,4,5-trisphosphate (IP3), norepinephrine and prostaglandin F2alpha produce larger enhancement of DNA synthesis. Inositol 1,4,5-Trisphosphate 209-212 angiotensinogen Homo sapiens 55-69 10361980-3 1999 We show that vasopressin and angiotensin II also cause a prolonged elevation of cellular IP3 levels. Inositol 1,4,5-Trisphosphate 89-92 angiotensinogen Homo sapiens 29-43 9757050-4 1998 When expressed in COS-7 cells, stimulation by Angiotensin II of both the cloned gerbil receptor or the human AT1 receptor enhanced IP3 production to a similar degree. Inositol 1,4,5-Trisphosphate 131-134 angiotensinogen Homo sapiens 46-60 9833159-11 1998 Microinjection of IP3 induced a [Ca++]i response in adjacent cells which was similar to the ANG II-induced effects. Inositol 1,4,5-Trisphosphate 18-21 angiotensinogen Homo sapiens 92-98 9453258-6 1997 In cultured RMICs, Ang II markedly increases intracellular inositol 1,4,5-triphosphate (IP3) concentration, and stimulates cell proliferation and extracellular matrix synthesis, and these cellular responses are exclusively mediated by AT1 receptors. Inositol 1,4,5-Trisphosphate 59-86 angiotensinogen Homo sapiens 19-25 9453004-6 1998 Angiotensin II (10(-6) M) increased intracellular IP3 concentrations at 20 seconds, and decreased intracellular cAMP concentrations after 10 minutes. Inositol 1,4,5-Trisphosphate 50-53 angiotensinogen Homo sapiens 0-14 9453258-6 1997 In cultured RMICs, Ang II markedly increases intracellular inositol 1,4,5-triphosphate (IP3) concentration, and stimulates cell proliferation and extracellular matrix synthesis, and these cellular responses are exclusively mediated by AT1 receptors. Inositol 1,4,5-Trisphosphate 88-91 angiotensinogen Homo sapiens 19-25 9279776-8 1997 Thus, either one of the Ang II-induced second messengers, that is, IP3 and DAG, has the potential to affect myocardial contractility by modifying either intracellular Ca2+, myofilament Ca2+ responsiveness, or both. Inositol 1,4,5-Trisphosphate 67-70 angiotensinogen Homo sapiens 24-30 9223623-4 1997 Angiotensin II also increased the resynthesis of phosphatidylinositol and the production of IP3. Inositol 1,4,5-Trisphosphate 92-95 angiotensinogen Homo sapiens 0-14 8952695-3 1996 AII also triggered a fast accumulation of IP3 and a rapid increase in [Ca2+]i in cells loaded with the Ca(2+)-responsive fluorescent dye fura-2. Inositol 1,4,5-Trisphosphate 42-45 angiotensinogen Homo sapiens 0-3 8952695-5 1996 The AII-triggered increases in IP3, [Ca2+]i, and Lucifer yellow uptake were inhibited by the nonselective AII receptor antagonist, Sar1, Val5, Ala8-AII (SVA-AII), and by the phospholipase C (PLC) inhibitors, neomycin and U-73122. Inositol 1,4,5-Trisphosphate 31-34 angiotensinogen Homo sapiens 4-7 8952695-5 1996 The AII-triggered increases in IP3, [Ca2+]i, and Lucifer yellow uptake were inhibited by the nonselective AII receptor antagonist, Sar1, Val5, Ala8-AII (SVA-AII), and by the phospholipase C (PLC) inhibitors, neomycin and U-73122. Inositol 1,4,5-Trisphosphate 31-34 angiotensinogen Homo sapiens 106-109 8952695-5 1996 The AII-triggered increases in IP3, [Ca2+]i, and Lucifer yellow uptake were inhibited by the nonselective AII receptor antagonist, Sar1, Val5, Ala8-AII (SVA-AII), and by the phospholipase C (PLC) inhibitors, neomycin and U-73122. Inositol 1,4,5-Trisphosphate 31-34 angiotensinogen Homo sapiens 106-109 8952695-5 1996 The AII-triggered increases in IP3, [Ca2+]i, and Lucifer yellow uptake were inhibited by the nonselective AII receptor antagonist, Sar1, Val5, Ala8-AII (SVA-AII), and by the phospholipase C (PLC) inhibitors, neomycin and U-73122. Inositol 1,4,5-Trisphosphate 31-34 angiotensinogen Homo sapiens 106-109 8947038-1 1996 Intracellular Ca2+ signalling evoked by Ca2+ mobilizing agonists, like angiotensin II in the adrenal gland, involves the activation of inositol(1,4,5)trisphosphate(InsP3)-mediated Ca2+ release from internal stores followed by activation of a Ca2+ influx termed capacitative calcium entry. Inositol 1,4,5-Trisphosphate 135-163 angiotensinogen Homo sapiens 71-85 2556386-5 1989 Release of the inositol 1,4,5-trisphosphate-sensitive Ca2+ pool by tBuBHQ following pretreatment with vasopressin or angiotensin II resulted in a [Ca2+]i transient and not the sustained [Ca2+]i elevation observed in the absence of the Ca2(+)-mobilizing hormones. Inositol 1,4,5-Trisphosphate 15-43 angiotensinogen Homo sapiens 117-131 8385928-7 1993 A working hypothesis is proposed in which vasopressin- or angiotensin II-induced spikes consist of an Ins(1,4,5)P3-mediated symmetrical spike, identical in time course and mechanism with those induced by phenylephrine, followed by a "tail" that represents CICR. Inositol 1,4,5-Trisphosphate 102-114 angiotensinogen Homo sapiens 58-72 1860709-4 1991 In contrast, angiotensin-(2-8) caused only a slight increase in prostaglandin release, even though it was as effective as angiotensin II in augmenting inositol 1,4,5-trisphosphate production and calcium mobilization. Inositol 1,4,5-Trisphosphate 151-179 angiotensinogen Homo sapiens 122-136 2154969-9 1990 In contrast, a similar incubation with cholera toxin markedly inhibited angiotensin II-stimulated IP2 and IP3 release by 67 +/- 6% and 62 +/- 6% respectively. Inositol 1,4,5-Trisphosphate 106-109 angiotensinogen Homo sapiens 72-86 34769164-8 2021 ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Inositol 1,4,5-Trisphosphate 114-117 angiotensinogen Homo sapiens 55-61 7515876-1 1994 Angiotensin II (AII) evokes a biphasic increase in inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) levels in adrenal glomerulosa cells, with an extracellular Ca(2+)-independent early peak followed by a secondary sustained elevation that is highly dependent on the presence of extracellular Ca2+. Inositol 1,4,5-Trisphosphate 51-79 angiotensinogen Homo sapiens 0-14 7515876-1 1994 Angiotensin II (AII) evokes a biphasic increase in inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) levels in adrenal glomerulosa cells, with an extracellular Ca(2+)-independent early peak followed by a secondary sustained elevation that is highly dependent on the presence of extracellular Ca2+. Inositol 1,4,5-Trisphosphate 51-79 angiotensinogen Homo sapiens 16-19 7515876-1 1994 Angiotensin II (AII) evokes a biphasic increase in inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) levels in adrenal glomerulosa cells, with an extracellular Ca(2+)-independent early peak followed by a secondary sustained elevation that is highly dependent on the presence of extracellular Ca2+. Inositol 1,4,5-Trisphosphate 81-94 angiotensinogen Homo sapiens 0-14 7515876-1 1994 Angiotensin II (AII) evokes a biphasic increase in inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) levels in adrenal glomerulosa cells, with an extracellular Ca(2+)-independent early peak followed by a secondary sustained elevation that is highly dependent on the presence of extracellular Ca2+. Inositol 1,4,5-Trisphosphate 81-94 angiotensinogen Homo sapiens 16-19 7515876-5 1994 Also, there was an accumulation of Ins(1,4,5)P3 and diminished formation of Ins(1,3,4,5)P4 and Ins(1,3,4)P3 when intact glomerulosa cells were stimulated by AII in the presence of Sr2+. Inositol 1,4,5-Trisphosphate 35-47 angiotensinogen Homo sapiens 157-160 8132619-5 1994 NPY attenuated AII- or BK-induced inositol 1,4,5-trisphosphate production, and herbimycin A reversed this NPY effect. Inositol 1,4,5-Trisphosphate 34-62 angiotensinogen Homo sapiens 15-18 8498970-3 1993 Angiotensin II (Ang II) causes (AT1)-receptor mediated stimulation of phospholipase C, resulting in generation of IP3 (inositol triphosphate) and activation of protein kinase C, elevated cytosolic Ca+ and stimulation phospholipase A2. Inositol 1,4,5-Trisphosphate 114-117 angiotensinogen Homo sapiens 0-14 8498970-3 1993 Angiotensin II (Ang II) causes (AT1)-receptor mediated stimulation of phospholipase C, resulting in generation of IP3 (inositol triphosphate) and activation of protein kinase C, elevated cytosolic Ca+ and stimulation phospholipase A2. Inositol 1,4,5-Trisphosphate 114-117 angiotensinogen Homo sapiens 16-22 1860709-2 1991 The addition of angiotensin II to CRTG3 cells resulted in a dose-dependent release of prostaglandin E2 and prostacyclin, the production of inositol 1,4,5-trisphosphate, and the mobilization of intracellular calcium. Inositol 1,4,5-Trisphosphate 139-167 angiotensinogen Homo sapiens 16-30 2673302-2 1989 Activation of vascular smooth muscle by angiotensin II results in the phospholipase C-mediated generation of two second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG). Inositol 1,4,5-Trisphosphate 156-159 angiotensinogen Homo sapiens 40-54 2547768-1 1989 In adrenal glomerulosa cells, angiotensin II (AII) rapidly stimulates the formation of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and causes marked long-term changes in the levels of highly phosphorylated inositols. Inositol 1,4,5-Trisphosphate 87-115 angiotensinogen Homo sapiens 30-44 2547768-1 1989 In adrenal glomerulosa cells, angiotensin II (AII) rapidly stimulates the formation of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and causes marked long-term changes in the levels of highly phosphorylated inositols. Inositol 1,4,5-Trisphosphate 87-115 angiotensinogen Homo sapiens 46-49 2547768-1 1989 In adrenal glomerulosa cells, angiotensin II (AII) rapidly stimulates the formation of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and causes marked long-term changes in the levels of highly phosphorylated inositols. Inositol 1,4,5-Trisphosphate 117-129 angiotensinogen Homo sapiens 30-44 2547768-1 1989 In adrenal glomerulosa cells, angiotensin II (AII) rapidly stimulates the formation of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and causes marked long-term changes in the levels of highly phosphorylated inositols. Inositol 1,4,5-Trisphosphate 117-129 angiotensinogen Homo sapiens 46-49 2673302-7 1989 This guanine nucleotide regulatory protein, movement of the receptor-ligand complex, and the signals generated by the two second messengers, IP3 and DG, interact in a complex manner to cause an integrated response of vascular smooth muscle to angiotensin II stimulation. Inositol 1,4,5-Trisphosphate 141-144 angiotensinogen Homo sapiens 243-257 3283118-0 1988 Angiotensin II and guanine nucleotides stimulate formation of inositol 1,4,5-trisphosphate and its metabolites in permeabilized adrenal glomerulosa cells. Inositol 1,4,5-Trisphosphate 62-90 angiotensinogen Homo sapiens 0-14 3283118-1 1988 Angiotensin II (AII) interacts with specific receptors in the adrenal glomerulosa cell and stimulates the hydrolysis of plasma membrane phosphoinositides by phospholipase C, with production of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and subsequent mobilization of intracellular Ca2+. Inositol 1,4,5-Trisphosphate 193-221 angiotensinogen Homo sapiens 0-14 3283118-1 1988 Angiotensin II (AII) interacts with specific receptors in the adrenal glomerulosa cell and stimulates the hydrolysis of plasma membrane phosphoinositides by phospholipase C, with production of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and subsequent mobilization of intracellular Ca2+. Inositol 1,4,5-Trisphosphate 193-221 angiotensinogen Homo sapiens 16-19 3283118-1 1988 Angiotensin II (AII) interacts with specific receptors in the adrenal glomerulosa cell and stimulates the hydrolysis of plasma membrane phosphoinositides by phospholipase C, with production of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and subsequent mobilization of intracellular Ca2+. Inositol 1,4,5-Trisphosphate 223-235 angiotensinogen Homo sapiens 0-14 3283118-1 1988 Angiotensin II (AII) interacts with specific receptors in the adrenal glomerulosa cell and stimulates the hydrolysis of plasma membrane phosphoinositides by phospholipase C, with production of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and subsequent mobilization of intracellular Ca2+. Inositol 1,4,5-Trisphosphate 223-235 angiotensinogen Homo sapiens 16-19 3283118-6 1988 In addition to Ins-1,4,5-P3 and its metabolites formed during degradation via the 4-monophosphate pathway, AII and GTP gamma S stimulated the formation of the phosphorylated metabolite inositol 1,3,4,5-tetrakisphosphate and inositol 1,3,4-trisphosphate in permeabilized cells. Inositol 1,4,5-Trisphosphate 15-27 angiotensinogen Homo sapiens 107-110 2854052-7 1988 Serotonin, histamine, and angiotensin II produced higher levels of inositol phosphates (IP, IP2, IP3) in SMC than in endothelium. Inositol 1,4,5-Trisphosphate 97-100 angiotensinogen Homo sapiens 26-40 3078271-2 1988 Activation of vascular smooth muscle by angiotensin II results in the generation of two second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG). Inositol 1,4,5-Trisphosphate 131-134 angiotensinogen Homo sapiens 40-54 3078271-10 1988 Angiotensin II-stimulated, phospholipase C-mediated IP3 formation is also modulated by a pertussis toxin-insensitive guanine nucleotide regulatory protein. Inositol 1,4,5-Trisphosphate 52-55 angiotensinogen Homo sapiens 0-14 3078271-12 1988 The GTP binding protein, movement of the receptor-ligand complex, and the signals generated by the two second messengers, IP3 and DG, interact in a complex manner to cause an integrated response of vascular smooth muscle cells to angiotensin II stimulation. Inositol 1,4,5-Trisphosphate 122-125 angiotensinogen Homo sapiens 230-244 3104319-13 1987 These results suggest that, upon termination of angiotensin II action, calcium is rapidly accumulated first in an intracellular pool which is insensitive to either inositol 1,4,5-trisphosphate or arachidonic acid and that the trigger pool is restored gradually thereafter. Inositol 1,4,5-Trisphosphate 164-192 angiotensinogen Homo sapiens 48-62 26850364-7 2016 Using inhibitory analysis and selective antagonists, we now show that Ang II initiates periodic Sa(2+)-oscillations and transient responses by activating AT1 and AT2 receptors and involving branched signaling cascades: 1) Ang II Gq PLC IP3 IP3Rs Ca(2+) 2) Gbetagamma PI3Kgamma PKB 3) PKB eNOS NO PKG 4) CD38 cADPR RyRs Ca(2+) In these cascades, AT1 receptors play the leading role. Inositol 1,4,5-Trisphosphate 242-245 angiotensinogen Homo sapiens 70-76 3015563-4 1986 Angiotensin II (ATII) also induced glomerulosa cells to produce a dose-dependent (up to 10-fold) increase in IP, IP2, and IP3, but had only a small effect on fasciculata cells. Inositol 1,4,5-Trisphosphate 122-125 angiotensinogen Homo sapiens 0-14 2426266-10 1986 Treatment of hepatocytes with PMA likewise inhibits the ability of vasopressin, angiotensin II, and alpha 1-adrenergic agonists to increase IP3 and mobilize Ca2+ (Lynch, C. J., Charest, R., Bocckino, S. B., Exton, J. H., and Blackmore, P. F. (1985) J. Biol. Inositol 1,4,5-Trisphosphate 140-143 angiotensinogen Homo sapiens 80-94 2579567-1 1985 Receptor occupation by a variety of Ca2+-mobilizing hormones, such as alpha 1-adrenergic agents, vasopressin and angiotensin II, causes a rapid phosphodiesterase-mediated hydrolysis of phosphatidylinositol-4,5-bisphosphate in the plasma membrane with the production of the water soluble compound myo-inositol-1,4,5-trisphosphate (IP3) and the lipophilic molecule 1,2-diacylglycerol (DG). Inositol 1,4,5-Trisphosphate 296-328 angiotensinogen Homo sapiens 113-127 2579567-1 1985 Receptor occupation by a variety of Ca2+-mobilizing hormones, such as alpha 1-adrenergic agents, vasopressin and angiotensin II, causes a rapid phosphodiesterase-mediated hydrolysis of phosphatidylinositol-4,5-bisphosphate in the plasma membrane with the production of the water soluble compound myo-inositol-1,4,5-trisphosphate (IP3) and the lipophilic molecule 1,2-diacylglycerol (DG). Inositol 1,4,5-Trisphosphate 330-333 angiotensinogen Homo sapiens 113-127 6238962-2 1984 In the present study, it was shown that AII induces the rapid (10 s) hydrolysis of phosphatidylinositol 4-phosphate and -4,5-bisphosphate, leading to the sustained production of inositol bis- and trisphosphate (Ins-P3), and diacylglycerol rich in arachidonic acid. Inositol 1,4,5-Trisphosphate 211-217 angiotensinogen Homo sapiens 40-43