Potassium supplementation has been shown to decrease blood pressure in human and animal models of hypertension. The purpose of this study was to determine if potassium supplementation altered sympathetic nerve activity by altering 3H-norepinephrine release in caudal artery preparations of spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Supplementation in the drinking water with 0.5 or 1.0% KCl for 5 weeks lowered blood pressure (19 and 25 mm Hg, respectively) in SHR but had no effect on WKY. The decrease in blood pressure with 0.5% KCl was not accompanied by significant changes in either plasma or cerebrospinal fluid (CSF) sodium or potassium levels in either SHR or WKY. 3H-Norepinephrine release induced by 56 mmol/l KCl was not altered in either SHR or WKY. However, the ability of yohimbine to enhance 3H-norepinephrine release in caudal artery preparations was significantly decreased by potassium supplementation in SHR, but was not affected in WKY. These data suggest that potassium supplementation may alter α2-adrenoceptor activity. Further studies are required to determine if this altered α2-adrenoceptor activity plays a direct role in the blood-pressure-lowering effects of potassium supplementation.

Keywords:
Potassium, Spontaneously hypertensive rats, Blood pressure, 3H-Norepinephrine release, Caudal artery
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© 1990 S. Karger AG, Basel
1990
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