ALTERATIONS IN RAT INTERLOBAR ARTERY MEMBRANE-POTENTIAL AND K+ CHANNELS IN GENETIC AND NONGENETIC HYPERTENSION

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, f ew 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 Ca2+-imaging fluorescence were used to e xamine the differences in Wistar-Kyoto (WKY), Sprague-Dawley (SD), spo ntaneously hypertensive (SHR), and deoxycorticosterone acetate (DOCA) hypertensive single cells of rat kidney interlobar arteries. In curren t-clamp experiments, SHR and DOCA hypertensive cells were approximate to 20 mV more depolarized than the control cells. In voltage-clamp exp eriments with 4-aminopyridine and niflumic acid present to inhibit vol tage-dependent K+ (K-(v)) and Ca2+-activated Cl- (Cl-(Ca)) currents, S HR and DOCA hypertensive Ca2+-activated K+ (K-(Ca)) currents were sign ificantly larger and activated at more negative potentials than the co ntrol. Conversely, with charybdotoxin and niflumic acid present to inh ibit K-(Ca) and Cl-(Ca) currents, SHR and DOCA hypertensive K-(v) curr ent was significantly smaller than the control. Finally, basal and ang iotensin II-stimulated peak intracellular free [Ca2+] was greater in t he 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 arter ies and may play a role in the regulation of renal blood flow under ph ysiological and pathophysiological conditions.