Mechanism of the antihypertensive effect of K depletion in the spontaneously hypertensive rat

摘要

Mechanism of the antihypertensive effect of K depletion in the spontaneously hypertensive rat. K depletion reverses hypertension in the SHR (systolic blood pressure: K deplete 122 5 vs. K replete 164 4 mm Hg, P max) (156 20 vs. 81 5 fmol/mg of protein, P max were still increased in nephrectomized K depleted SHR. To determine the specific effect of K depletion independent of Ang II on Ang II binding, studies were performed in mesenteric artery VSMC from SHR grown in culture. VSMC from K replete SHR were grown to confluency in K replete medium and then were incubated in K depleted medium for 24 hours. Binding was saturable, time and temperature-dependent in K replete and K depleted cells. Total binding and Bmax (139 13 vs. 93 7 fmol/mg protein, P < 0.01) were increased in K depleted cells. The protective effect of K depletion in SHR is mediated by a decrease in vascular responsiveness to Ang II. Since Ang II binding is increased in both K depleted mesenteric arteries and in K depleted VSMC, the decrease in vascular responsiveness is the result of a K depletion-induced post-binding defect.