Hypertension, Vol 13, 676-680, Copyright © 1989 by American Heart Association
JM Smith, EJ Cragoe and AW Jones
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)
ARTICLES
Nisoldipine inhibition of sodium influx into aorta from aldosterone- salt-hypertensive rats
Department of Physiology, University of Missouri, Columbia 65212.
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