Ca and Na interaction in vascular smooth muscle contraction

Sitrin,; Df, Bohr

doi:10.1152/ajplegacy.1971.220.4.1124

Cited by 78 publications

(22 citation statements)

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“…In the rat uterus preparation, the contractile response to All showed a phasic component which may have been triggered by Ca2" influx and a tonic phase which the authors suggested was due to the release of Ca2" sequestered within the cell (8). The higher permeability of the cell to Na+ might increase free Ca2+ via a Na+/Ca2+ exchange as discussed by Blaustein and others (24)(25)(26)(27)(28). Alternatively, depolarization might activate a Ca2" transporter that is regulated by the membrane potential (28).…”

Section: Discussionmentioning

confidence: 91%

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

Brock¹,

Lewis²,

Smith³

1982

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin markedly altered the Na' permeability of smooth muscle cells cultured from explants of rat aorta. The rate ofnet Na' uptake was followed in the presence ofouabain in order to block Na' efflux via the Na+/K' pump. Angiotensin H (All) or angiotensin m (AHI) increased net Na' uptake by about 3-fold. Maximal stimulation of Na' uptake was produced by about 10 nM AUl. Bradykinin and the angiotensin antagonist [Sari, Ileu5, Ala8JAII had no significant effect on net Na+ uptake. Angiotensin also enhanced the activity of the Na+/K+ pump, which was assayed by following the rate of ouabain-sensitive wRb+ uptake by the cells. AII and AI nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [SariIleu5,Ala8]AII had no effect. In the presence of ouabain, 86Rb+ uptake was not significantly affected by AUl or AM, indicating that angiotensin did not alter passive permeability to Rb+. Loading the cells with Na+, either by incubation in K+-free medium or exposure to the Na+-selective ionophore monensin, markedly increased ouabainsensitive 86Rb+ uptake. This result indicates that the activity ofthe Na+/K+ pump is limited by the low level of Na+ that is normally in the cells. All had no effect on the activity of the Na+/K+ pump in Na+-loaded cells. These results suggest that All or AIM stimulates the Na+/K+ pump in cultured aortic muscle cells by increasing its Na+ supply.The octapeptide hormone angiotensin II (All) is a highly potent vasoconstrictor (1-3). Specific receptors on the surface of smooth muscle cells (4) mediate the contractile response to All, which occurs when the level of free Ca2" in the cytoplasm increases (5, 6). It is unclear what transmembrane events are elicited when All binds to its receptor on the cell surface.All is known to depolarize the smooth muscle membrane in various tissues (7)(8)(9). Recently, Hamon and Worcel (9) reported evidence suggesting that All depolarizes uterine smooth muscle by increasing the conductance of the membrane to Na+. Alterations in Na+ permeability also appear to be involved in vasoconstriction by angiotensin. Increasing the Na+ concentration in the medium bathing segments of rat aorta potentiates the contractile response to All (10), and perfusing rat tail arteries with low Na+ decreases the constriction elicted by All (11). However, the reported influences of angiotensin on the Na+ movements in isolated vascular tissue are ambiguous. Although Friedman and Allardyce (12) reported that angiotensin decreased the Na' activity in the medium bathing an artery, Guignard and Friedman (13) found that pressor doses ofAll had no such effect.All was recently shown to stimulate phosphorylation of the 20,000-dalton light chain of myosin in primary cultures of vascular smooth muscle (14). Therefore, it is feasible to study vasoactive mechanisms in cultured cells. In an attempt to elucidate further the effects of angiotensin on cation transport, we have examined the influence of vasoactive agents on Na' and K+ movements in cultures of rat aor...

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Section: Discussionmentioning

confidence: 91%

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

Brock¹,

Lewis²,

Smith³

1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Indomethacin reduced the effects of such combinations of depolarizing agents to that obtained with hydrogen peroxide in BSF. Indomethacin failed to modify the depolarizing effect of a combination of hydrogen peroxide with either cuprous or potassium ions ( (Daly & Clark, 1921;Luttgau & Niedergerke, 1958;Bohr, Seidel & Sobieski, 1969;Sitrin & Bohr, 1971). The ability of sodium ions to oppose the depolarizing effect of calcium ions on heated endothelial cells, therefore, is probably due to competition between the two cations for occupation of a cellular binding site which is important for the regulation of the membrane potential.…”

Section: Resultsmentioning

confidence: 99%

INTERACTION OF MONO‐ AND DIVALENT METALLIC CATIONS AND OF INDOMETHACIN ON THE MEMBRANE POTENTIAL OF VASCULAR ENDOTHELIAL CELLS in vitro

Northover

1975

British J Pharmacology

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Polytechnic, Leicester LE1 9BH 1 Endothelial cells depolarized progressively when heated for 5 h at 45 C in the presence of calcium (1 mM), cupric (0.08 mM) or ferrous (0.04 mM) ions. In the absence of these ions, heating caused only slight depolarization. Higher concentrations of these ions caused depolarization even at normal body temperature (37" C).2 Cuprous and potassium ions, although producing depolarization at 37 C, failed to augment the depolarization due to heating to 45 C. 3 Hydrogen peroxide caused depolarization which was potentiated by the presence of calcium, cupric or ferrous ions, but not by the presence of cuprous or potassium ions. 4 Indomethacin (0.25 mM) reduced the depolarization caused by calcium, cupric or ferrous ions at 370 C and also reduced the potentiation of heat-induced and hydrogen peroxide-induced depolarization which these divalent metallic cations produced. However, indomethacin failed to modify the depolarization caused by cuprous or potassium ions.

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“…47 -4 * The relation is parabolic. This reduction in vascular reactivity with increasing concentrations of extracellular calcium has been ascribed in part to a membrane stabilizing effect of the cation 46 …”

Section: Vascular Reactivity and Blood Pressure Response To Calcium Amentioning

confidence: 99%

Is calcium more important than sodium in the pathogenesis of essential hypertension?

McCarron¹

1985

Hypertension

161

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SUMMARY The hypothesis that abnormalities of calcium homeostasis at both an organ and cellular level are a primary factor in the pathogenesis of human and experimental hypertension forms the basis of this review. The rapidly expanding data base relating disordered calcium metabolism to altered vascular smooth muscle function and increased peripheral vascular resistance is summarized and integrated with the observations that reduced dietary calcium intake is the most consistent nutritional correlate of hypertension in the United States. The role of sodium and sodium chloride in pathogenesis of hypertension is reassessed in the light of new data from epidemiological clinical research, experimental models, and cell physiology investigations. The data supporting the thesis that the effects of sodium or chloride or both on blood pressure may represent, in selected situations, secondary influences mediated through induced changes in calcium homeostasis are presented. The interface between these nutritional factors and the normal regulation of vascular smooth muscle is discussed, providing a theoretical framework in which to assess the current information and to formulate the necessary future research. (Hypertension 7: 607-627, 1985) KEY WORDS • calcium • sodium • vascular smooth muscle cells • spontaneously hypertensive rats • deoxycorticosterone acetate rat • calmodulin • Ca -activated adenosine triphosphatase * nutrition F EW concepts in medicine are more widely accepted than the theoretical link between dietary sodium and the pathogenesis of essential hypertension.l-) In spite of this perceived consensus, however, many investigators have remained skeptical of the notion that sodium or a defect in sodium balance, or both, is the principal cause of high blood pressure in most humans with essential hypertension.

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Ca and Na interaction in vascular smooth muscle contraction

Cited by 78 publications

References 0 publications

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

INTERACTION OF MONO‐ AND DIVALENT METALLIC CATIONS AND OF INDOMETHACIN ON THE MEMBRANE POTENTIAL OF VASCULAR ENDOTHELIAL CELLS in vitro

Is calcium more important than sodium in the pathogenesis of essential hypertension?

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