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 M Na influx was elevated in aorta from the hypertensive rats (2.21+0.10 mmol/1 cell H 2 0/min, n=25) compared with control-salt rats (1.75±0.04 mmol/1 cell H 2 O/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/1 ceU H 2 0/min, n=10) was similar to control rats (1.66±0.18 mmol/1 cell H 2 0/min, n=l). 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/1 cell H 2 O/min for basal (n=25), dichlorobenzamil (w=4), and ethylisoproisopropylamiloride (n=ll), respectively. Inhibition of Na influx in hypertensive rats by 0.1 fiM nisoldipine (ANa influx=-0.72±0.18 mmol/1 cell H 2 0/min, n=9) was not significantly altered when applied with dichlorobenzamil (-0.72±0.21 mmol/1 cell H 2 O/min, n=4) or ethylisopropylamiloride (-0.55±0.15 mmol/1 cell H 2 O/min, n = l l ) . These agents did not alter Na influx in control aorta. Our results suggest that, in aorta from aldosterone-salt-hypertensive rats, an elevated Na influx exists that is dependent on Ca entry through potential-operated Ca channels. Na-Ca and Na-H exchange do not appear to contribute significantly to the elevated Na influx, which is suggested to result from the activity of a Ca-dependent cationic channel. (Hypertension 1989;13:676-680)