Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats - PubMed (original) (raw)

Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats

J M Smith et al. Hypertension. 1990 Jan.

Abstract

The purpose of this study was to evaluate the effect of calcium antagonists on basal tension and the elevated 42K efflux in aorta from aldosterone-salt hypertensive rats. Diltiazem decreased the basal tension (2.0 +/- 0.4 g) as well as the phasic contractile activity and returned the elevated 42K efflux (0.018 +/- 0.002/min) toward control values (0.010 +/- 0.001/min, p less than 0.001). The diltiazem median inhibitory concentration (IC50) for basal tension (0.04 +/- 0.02 microM), however, was sevenfold less than the IC50 for basal 42K efflux (0.22 +/- 0.08 microM, p less than 0.01). The basal 45Ca influx in aorta from aldosterone-salt hypertensive rats (120 +/- 4 microM/l cell H2O/min) was also decreased by diltiazem in a concentration-dependent manner, whereas the 45Ca influx in aorta from control-salt rats (135 +/- 3 microM/l cell H2O/min) was not altered. Similarly, the dihydropyridine nisoldipine eliminated the basal tension (2.7 +/- 0.5 g) and returned the elevated basal 42K efflux from the hypertensive aorta toward control levels (0.010 +/- 0.0003/min, p less than 0.001). The nisoldipine IC50 for basal tension (0.016 +/- 0.01 nM) was 160-fold less than the IC50 for basal 42K efflux (1.8 +/- 1.2 nm, p less than 0.001). Neither diltiazem nor nisoldipine nisoldipine altered the basal 42K efflux or contractile activity of aorta from control-salt rats. These results suggest that the basal tension and elevated 42K efflux in aorta from aldosterone-salt hypertensive rats are supported by the entry of extracellular calcium into the tissue through potential-operated calcium channels.

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