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 ≈20 mV more depolarized than the control cells. In voltage-clamp experiments with 4-aminopyridine and niflumic acid present to inhibit voltage-dependent K + (K (v) ) and Ca 2+ -activated Cl − (Cl (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 Cl (Ca) currents, SHR and DOCA hypertensive K (v) current was significantly smaller than the control. Finally, basal and angiotensin II–stimulated peak intracellular free [Ca 2+ ] 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 pathophysiological conditions.