Possible role of phosphorylation-dephosphorylation in the regulation of calcium metabolism in cardiovascular tissues of SHR.

Bhalla, Ramesh C.; Sharma, Ram V.; Ramanathan, S.

doi:10.1161/01.hyp.2.2.207

Cited by 13 publications

(1 citation statement)

References 27 publications

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“…For exam ple, the smooth muscle cells of the SHR aorta are reported to have an increased passive per meability to sodium and potassium [Jones, 1973]; there is some evidence for an increase in the Na,K-ATPase activity of smooth mus cle cells of tail artery from SHRs [Hermsmeyer, 1976;Pamnani et al, 1980]. suggest ing that differences in the sodium pump may be involved [Fleming, 1980]; the calcium binding capacity of the plasma membrane of smooth muscle cells from aorta [Zsoteret al, 1977;Bhalla et al, 1978]; superior mesen teric artery [Wei et al, 1976] and tail artery [Bhalla et al, 1980] is less in SHRs than in WKYs. This suggests that there could be ab normalities in the membranes ofSHR vascu lar smooth muscle cells, and indeed it has been proposed that membrane abnormalities could be a cause of hypertension [Blaustein, 1977], It is to be hoped that techniques for investigating membrane properties in the smooth muscle of small vessels will be devel oped as soon as possible.…”

Section: Isolated Resistance Vesselsmentioning

confidence: 99%

Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Mulvany¹

1983

J Vasc Res

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This review summarizes some of the evidence pointing to the existence of vascular abnormalities in the spontaneously hypertensive rat (SHR) and the extent to which such abnormalities could be responsible for the elevated blood pressure in this animal. Compared with its genetic normotensive control, the Wistar-Kyoto rat (WKY), the adult SHR has an increased total peripheral resistance (TPR). Many factors appear to contribute to the increased TPR, including an active rarefication of the vascular bed and a general constriction of the vasculature. There is evidence that the general constriction is due to structural differences in the resistance vessels, to abnormally high activation levels (i.e. increased sympathetic nerve activity), and to abnormal excitation-contracting coupling within the vasculature itself (i.e. increased noradrenaline sensitivity of the vascular smooth muscle cells). Age studies and studies of the effects of antihypertensive treatment suggest that both structural and excitation-contraction abnormalities may be present before the onset of hypertension.

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