Sodium pump activity and contraction of renal artery from spontaneously hypertensive rats

We investigated the hypertensive changes in renal arteries isolated from 21-week-old spontaneously hypertensive rats (SHR), and from age-matched normotensive Wistar-Kyoto rats (WKY). The maximum contraction of renal arteries from SHR in response to norepinephrine (NE), serotonin (5-HT) and KCl was greater than that of arteries from WKY. The threshold and EC50 concentrations of NE, 5-HT and KCl were not significantly different between SHR and WKY. Contraction induced by removal of K+ was inhibited by 10(-8) M prazosin. Less than 10(-7) M NE in K(+)-free solution did not cause contraction. Addition of 5.9 mM KCl to K(+)-free solution in the presence of 10(-5) M NE induced relaxation, which was followed by contraction to about the same level as that before KCl addition. The duration of the K(+)-induced relaxation in SHR (22.4 +/- 0.9 min) was slightly, but significantly shorter than that in WKY (26.6 +/- 0.8 min) arteries. In K(+)-free solution with reduced Na+, the duration of the relaxation induced by KCl was shorter than that in the normal solution, for both SHR (13.8 +/- 0.3 min) and WKY (14.1 +/- 0.5 min). Such differences could be caused by increased influx and decreased efflux of Ca2+, which depend on the Na+ concentration and are related to the Na(+)-Ca2+ exchange. The results suggest that enhanced renal vascular reactivity in hypertension may depend on structural changes and increased Na+ pump activity.