Growth rate and phospholipase C activity in cardiac and aortic spontaneously hypertensive rat cells

Millanvoye, Elisabeth; Freyss-Beguin, M; Baudouin-Legros, Maryvonne; Paquet, Jean‐Luc; Marché, P.; Durant, Sylvie; Meyer, Philippe

doi:10.1097/00004872-198812040-00115

Cited by 15 publications

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“…However, the phosphatidyl inositol cycle is complex with many intermediates and although TP3 is the key metabolite, others, in particular inositol 1345 tetrakisphosphate, may modulate cell calcium [14, 151. Several [19] observed an increase in inositol phosphate formation in stroke prone SHR. Increased angiotensin I1 stimulated inositol phosphate formation has been observed in cultured smooth muscle cells from SHR [20], while Paquet et al [21] have shown increased serotonin stimulated inositol phosphate formation in cultured aortic smooth muscle cells from SHR suggesting that, in this case, cultured cells may reflect what is occurring in the whole artery.…”

Section: Introductionmentioning

confidence: 96%

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

et al. 1993

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Total [3H]-inositol phosphate formation was measured in cultured aortic smooth muscle cells from 6 and 14 week spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) normotensive rats. Basal inositol phosphate formation was significantly increased in cells cultured from SHR compared to WKY at both 6 and 14 weeks as was basal phosphatidylinositol formation. This difference in basal values was apparent after 9 h or more incubation with [3H]-myoinositol. Both endothelin-1 and noradrenaline stimulated inositol phosphate formation was unchanged in cultured smooth muscle cells from 6-week SHR compared to WKY. In cultured smooth muscle cells from 14-week SHR a decrease was observed in endothelin-1 stimulated inositol phosphate formation compared to controls. Noradrenaline stimulated inositol phosphate formation was increased in cultured cells from 14 week SHR. Endothelin-1 and noradrenaline stimulated inositol phosphate formation does not appear to be involved in the development (at 6 weeks) of hypertension in this model. However, in established hypertension (14 weeks) cells from SHR have altered total [3H] inositol phosphate formation in response to stimulation with noradrenaline and endothelin-1 although these changes are in opposite directions. Therefore, in cultured smooth muscle cells from 14-week rats noradrenaline and endothelin-1 appear to be regulated independently with regard to their effects on the phosphatidylinositol cycle.

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Section: Introductionmentioning

confidence: 96%

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

et al. 1993

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“…First, because the PLC pathway may be a source of AA release caused by shear stress in VSMC, and because several publications (22)(23)(24)(25)(26)(27) have demonstrated enhanced PLC activity in VSMC obtained from SHR, the increases in shear-induced prostacyclin production in SHR VSMC may be due to increased PLC activity. Second, flow-induced NO production was less in SHR than in WKY.…”

Section: Discussionmentioning

confidence: 99%

Interaction between Flow-Induced Prostacyclin Production and Nitric Oxide Synthesis in Vascular Smooth Muscle Cells.

et al. 1994

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The interaction between flow-induced prostacyclin production and nitric oxide (NO) synthesis in vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) was studied. Flow was made by 3 cm-amplitude horizontal shaking at various frequencies at 37 °C under 5% CO 2 and 95% air. Basal prostacyclin and NO production rates did not differ between strains. Prostacyclm production during flow was significantly greater with increasing shear stress from shaking frequencies of 120/min to 180/min, and was greater in SHR than in WKY. In contrast, flow-induced NO production was greater in WKY than in SHR. The addition of N nitro-L-arginine further increased the flow-induced increase in the production of prostacyclin in WKY in a dose-dependent manner, but had no effects in SHR. Indomethacin did not affect flow-induced NO production in either strain. We conclude that increases in prostacyclin production in SHR-derived VSMC during shear stress may be due to decreases in the suppression by NO and may compensate for hypertension.(Hypertens Res 1994;17: 227-232) Key Words: spontaneously hypertensive rat, shear stress, prostacyclin, nitric oxide, vascular smooth muscle cell Prostacyclin, a potent vasodilator and the most potent endogenous inhibitor of platelet aggregation known, is synthesized from arachidonic acid (AA) in many types of cells. In vascular endothelial cells, mechanical forces associated with blood flow, such as shear stress and pressure-stretch, are known to stimulate prostacyclin production(1), and play an important role in the regulation of vascular tone (2), vascular remodeling (3), and the focal development of atherosclerotic lesions (4) . Shear stress also stimulates the production of nitric oxide (NO) via a shear-sensitive K current (5,6) in endothelial cells. Although previous studies of the effect of shear stress on prostacyclin or NO production were focused on vascular endothelial cells, vascular smooth muscle cells (VSMC) are also exposed to shear stress, such as blood flow when intima is exfoliated, and interstitial fluid flow during skeletal muscle contraction or relaxation. Moreover, previous evidence (7,8) has shown that shear stress caused by blood flow displaces the inner layers of the artery wall in the direction of flow as well as the endothelium, and that ion transport is more sensitive to shear in VSMC than in several other types of cells, including endothelial cells.Previous studies have shown that in VSMC shear stress opens nitrendipine-sensitive calcium channels (8), stimulates cell growth (9), and induces endocytosis of large amounts of extracellular sodium and cholesterol (9). Recent evidence (10) has shown that shear stress reduces the 24-hour incorporation of tritiated thymidine and cell proliferation. However, none of those studies addressed the effects of shear stress on production of prostacyclin and NO in VSMC. Because recent evidence (11) has shown that these compounds are also synthesized in VSMC and regulate the proliferation rates and ...

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“…TRPM4 is an intriguing potential contributor to this pathophysiological condition, as several of the molecular pathways that regulate its activity have also been shown to be altered under these conditions. For example, PLC activity and the generation of IP 3 increase in response to intraluminal pressures [64], and basal intracellular IP 3 concentrations are elevated in genetically hypertensive rats [7,58,83,98,100,104]. Although no difference in IP 3 R expression or IP 3 R-mediated Ca 2+ release has been reported, an increase in intracellular IP 3 level together with elevated cytosolic Ca 2+ levels could increase tonic IP 3 Rmediated TRPM4 channel activity and membrane depolarization.…”

Section: Trpm4 In Hypertensionmentioning

confidence: 99%

Regulation of Cerebral Artery Smooth Muscle Membrane Potential by Ca²⁺‐Activated Cation Channels

Gonzales

Earley

2013

Microcirculation

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Arterial tone is dependent on the depolarizing and hyperpolarizing currents regulating membrane potential and governing the influx of Ca2+ needed for smooth muscle contraction. Several ion channels have been proposed to contribute to membrane depolarization, but the underlying molecular mechanisms are not fully understood. In this review, we will discuss the historical and physiological significance of the Ca2+-activated cation channel, TRPM4, in regulating membrane potential of cerebral artery smooth muscle cells. As a member of the recently described transient receptor potential super family of ion channels, TRPM4 possesses the biophysical properties and upstream cellular signaling and regulatory pathways that establish it as a major physiological player in smooth muscle membrane depolarization.

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Growth rate and phospholipase C activity in cardiac and aortic spontaneously hypertensive rat cells

Cited by 15 publications

References 0 publications

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

Interaction between Flow-Induced Prostacyclin Production and Nitric Oxide Synthesis in Vascular Smooth Muscle Cells.

Regulation of Cerebral Artery Smooth Muscle Membrane Potential by Ca²⁺‐Activated Cation Channels

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Growth rate and phospholipase C activity in cardiac and aortic spontaneously hypertensive rat cells

Cited by 15 publications

References 0 publications

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

Comparison of Endothelin-1 and Noradrenaline Stimulated Inositol Phosphate Formation in Cultured Aortic Smooth Muscle Cells from Spontaneously Hypertensive and Wistar Kyoto Rats

Interaction between Flow-Induced Prostacyclin Production and Nitric Oxide Synthesis in Vascular Smooth Muscle Cells.

Regulation of Cerebral Artery Smooth Muscle Membrane Potential by Ca2+‐Activated Cation Channels

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Regulation of Cerebral Artery Smooth Muscle Membrane Potential by Ca²⁺‐Activated Cation Channels