Alterations in rat interlobar artery membrane potential and K+ channels in genetic and nongenetic hypertension.

Abstract

The renal vasculature plays an important role in the control of blood pressure. K+ channels have been demonstrated to regulate smooth muscle membrane potential and thereby control smooth muscle tone. However, few data are available on K+ channel function in the renal vasculature of hypertensive animals. This study details changes in K+ currents and membrane potential in genetic and nongenetic models of hypertension. The patch-clamp technique and Ca(2+)-imaging fluorescence were used to examine the differences in Wistar-Kyoto (WKY), Sprague-Dawley (SD), spontaneously hypertensive (SHR), and deoxycorticosterone acetate (DOCA) hypertensive single cells of rat kidney interlobar arteries. In current-clamp experiments, SHR and DOCA hypertensive cells were approximately 20 mV more depolarized than the control cells. In voltage-clamp experiments with 4-amino-pyridine and niflumic acid present to inhibit voltage-dependent K+ (K(v)) and Ca(2+)-activated CI- (CI(Ca)) currents, SHR and DOCA hypertensive Ca(2+)-activated K+ (K(Ca)) currents were significantly larger and activated at more negative potentials than the control. Conversely, with charybdotoxin and niflumic acid present to inhibit K(Ca) and CI(Ca) currents, SHR and DOCA hypertensive K(v) current was significantly smaller than the control. Finally, basal and angiotensin II-stimulated peak intracellular free [Ca2+] was greater in the SHR and DOCA hypertensive cells compared with control cells. These results suggest that membrane potential and the activity of K(Ca) and K(v) channels are altered in hypertensive rat renal interlobar arteries and may play a role in the regulation of renal blood flow under physiological and patho-physiological conditions.