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Hypertension. 1989;13:676-680

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Hypertension, Vol 13, 676-680, Copyright © 1989 by American Heart Association


ARTICLES

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

JM Smith, EJ Cragoe and AW Jones
Department of Physiology, University of Missouri, Columbia 65212.

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)