Nisoldipine inhibition of sodium influx into aorta from aldosterone-salt-hypertensive rats.

Abstract

The purpose of this study was to determine whether increased sodium (Na) influx into the aorta was associated with aldosterone-salt hypertension in the rat and, if present, to determine what mechanisms contributed to the increase. Basal 24Na influx was elevated in aorta from the hypertensive rats (2.21 +/- 0.10 mmol/l cell H2O/min, n = 25) compared with control-salt rats (1.75 +/- 0.04 mmol/l cell H2O/min, n = 24). The calcium (Ca) antagonist nisoldipine inhibited the Na influx into aorta from hypertensive rats in a concentration-dependent manner. At 10 nM nisoldipine, the Na influx in hypertensive rats (1.52 +/- 0.14 mmol/l cell H2O/min, n = 10) was similar to control rats (1.66 +/- 0.18 mmol/l cell H2O/min, n = 7). The basal Na influx in aorta from hypertensive rats was not altered by dichlorobenzamil or ethylisopropylamiloride, selective inhibitors of Na-Ca and Na-H exchange, respectively. The Na influx was 2.21 +/- 0.10, 2.03 +/- 0.24, and 2.11 +/- 0.19 mmol/l cell H2O/min for basal (n = 25), dichlorobenzamil (n = 4), and ethylisoproisopropylamiloride (n = 11), respectively. Inhibition of Na influx in hypertensive rats by 0.1 microM nisoldipine (delta Na influx = -0.72 +/- 0.18 mmol/l cell H2O/min, n = 9) was not significantly altered when applied with dichlorobenzamil (-0.72 +/- 0.21 mmol/l cell H2O/min, n = 4) or ethylisopropylamiloride (-0.55 +/- 0.15 mmol/l cell H2O/min, n = 11). These agents did not alter Na influx in control aorta.(ABSTRACT TRUNCATED AT 250 WORDS)