Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle.

Alexander, R. W.; Brock, T. A.; Gimbrone, M. A.; Rittenhouse, Susan E.

doi:10.1161/01.hyp.7.3_pt_1.447

Cited by 25 publications

(39 citation statements)

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“…Consistent with its role as a second messenger, the increase in the level of Insl ,4,5P3 was found to precede the onset of calcium-dependent events in blowfly salivary gland (20) and in neutrophils (21). Measurements of intracellular calcium in different cell types have revealed that the increase in Insl,4,5P3 either preceded (22 , 23) or coincided with the onset of the calcium signal (24)(25)(26)(27)(28). This evidence is consistent with the hypothesis that external signals act through a receptor mechanism to produce Insl,4,5P3, which then mobilizes calcium.…”

Section: Hydrolysis Of Ptdins45p2mentioning

confidence: 83%

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Berridge¹

1987

Annu. Rev. Biochem.

3,261

1,335

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Section: Hydrolysis Of Ptdins45p2mentioning

confidence: 83%

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Berridge¹

1987

Annu. Rev. Biochem.

3,261

1,335

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“…From the observation that target organs of A11 display slightly different response to A11 and A111 (Freer et al 1980;Trachte et al 1983), and different pathways of signal transduction (Alexander et al 1985;Pobiner et al 1985;Hausdorff et al 1988) the existence of subtypes of A11 receptors has been proposed. Recently, two distinct subtypes of the A11 receptor have been identified following the development of new nonpeptide A11 receptor antagonists.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Ii Receptor Subtypes in Rat Brain

Song

Allen

Paxinos

et al. 1991

Clin Exp Pharma Physio

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1. Angiotensin II (AII) receptor binding was localized in the rat brain by in vitro autoradiography using the antagonist analogue, 125I-[Sar1, Ile8] AII. AII receptor binding was then differentiated into type I and type II subtypes by displacement with unlabelled non-peptide antagonists specific for AII subtypes. 2. Type I binding was determined as that inhibited by Dup753 (10 mumol/L) and type II binding as that inhibited by XD329-1 (10 mumol/L). The reducing agent dithiothreitol (DTT) decreased the binding to type I receptors and enhanced the binding to type II receptors. 3. Structures such as the vascular organ of the lamina terminalis, subfornical organ, median preoptic nucleus, area postrema, nucleus of the solitary tract, which are known to be related to some central actions of AII, contain exclusively type I AII receptors. 4. In contrast, the locus coeruleus, ventral and dorsal parts of lateral septum, superior colliculus, subthalamic nucleus, some nuclei of the thalamus, and the nuclei of the inferior olive contain predominantly type II AII receptors. 5. These results reveal important pharmacological heterogeneity of brain AII receptors which suggest different regional functions and are relevant to the central actions of emerging classes of new non-peptide AII receptor antagonists.

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“…Intracellular Ca 2ϩ , as a global signal (18,19), leads to contraction of vascular smooth muscle cells (VSMCs) by binding to calmodulin and subsequent activation of myosin light chain kinases (36). A prominent mechanism for Ca 2ϩ release in smooth muscle cells is receptor-mediated activation of the inositol trisphosphate (IP 3 ) pathway (2,5). In contrast, cAMP relaxes VSMCs primarily by activation of protein kinase A (PKA, Ref.…”

mentioning

confidence: 99%

G_q-mediated Ca²⁺ signals inhibit adenylyl cyclases 5/6 in vascular smooth muscle cells

Hayn

Werthmann

Nikolaev

et al. 2010

American Journal of Physiology-Cell Physiology

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cAMP and Ca(2+) are antagonistic intracellular messengers for the regulation of vascular smooth muscle tone; rising levels of Ca(2+) lead to vasoconstriction, whereas an increase of cAMP induces vasodilatation. Here we investigated whether Ca(2+) interferes with cAMP signaling by regulation of phophodiesterases (PDEs) or adenylyl cyclases (ACs). We studied regulation of cAMP concentrations by Ca(2+) signals evoked by endogenous purinergic receptors in vascular smooth muscle cells (VSMCs). The fluorescence resonance energy transfer (FRET)-based cAMP sensor Epac1-camps allowed the measurement of cAMP levels in single-living VSMCs with subsecond temporal resolution. Moreover, in vitro calibration of Epac1-camps enabled us to estimate the absolute cytosolic cAMP concentrations. Stimulation of purinergic receptors decreased cAMP levels in the presence of the beta-adrenergic agonist isoproterenol. Simultaneous imaging of cAMP with Epac1-camps and of Ca(2+) with Fura 2 revealed a rise of intracellular Ca(2+) in response to purinergic stimulation followed by a decline of cAMP. Chelation of intracellular Ca(2+) and overexpression of Ca(2+)-independent AC4 antagonized this decline of cAMP, whereas pharmacological inhibition of Ca(2+)-activated PDE1 had no effect. AC assays with VSMC membranes revealed a significant attenuation of isoproterenol-stimulated cAMP production by the presence of 2 muM Ca(2+). Furthermore, small interfering RNA (siRNA) knockdown of AC5 and AC6 (the two ACs known to be inhibited by Ca(2+)), significantly reduced the decrease of cAMP upon purinergic stimulation of isoproterenol-prestimulated VSMCs. Taken together, these results implicate a Ca(2+)-mediated inhibition of AC5 and 6 as an important mechanism of purinergic receptor-induced decline of cAMP and show a direct cross talk of these signaling pathways in VSMCs.

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Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle.

Cited by 25 publications

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Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Angiotensin Ii Receptor Subtypes in Rat Brain

G_q-mediated Ca²⁺ signals inhibit adenylyl cyclases 5/6 in vascular smooth muscle cells

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Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle.

Cited by 25 publications

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Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Angiotensin Ii Receptor Subtypes in Rat Brain

Gq-mediated Ca2+ signals inhibit adenylyl cyclases 5/6 in vascular smooth muscle cells

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Product

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G_q-mediated Ca²⁺ signals inhibit adenylyl cyclases 5/6 in vascular smooth muscle cells