We investigated whether systemic and renal vasoconstriction induced by porcine endothelin (endothelin 1) is prevented by nifedipine in awake normotensive rats. Endothelin (0.07-1.4 nmol/kg iv) induced a long-lasting increase in mean blood pressure (MBP) and a decrease in renal blood flow (RBF). Maximal decrease in RBF was 25 ± 7% (0.07 nmol/kg), 40 ± 2 (0.35), 67 ± 5 (0.70), and 74 ± 8 (1.4). Hemodynamic parameters were back to base line within 35 ± 5 min (0.07 nmol/kg), 43 ± 6 (0.35), 60 ± 4 (0.70), and 81 ± 7 (1.4). Intravenous bolus injection of either angiotensin II (ANG II, 0.006-0.024 nmol/kg) or norepinephrine (0.40-1.60 nmol/kg) caused a dose-related short-lasting increase in MBP and a decrease in RBF. Endothelin was less potent than ANG II (1:3.42) and more potent than norepinephrine (1:0.015) as a renal vasoconstrictor. Nifedipine (1 mg/kg ip) was equally effective in preventing the increase in MBP caused by endothelin, norepinephrine, or ANG II. It exerted a weaker protection on the renal hemodynamic response to endothelin compared with the inhibition of the other two vasoconstrictors. Thus the regression line representing the relationship between endothelin-induced changes in MBP and RBF was steeper in rats given nifedipine (slope: vehicle, -1.33; nifedipine, -5.50; P <0.05). These studies suggest that nifedipine can partially prevent systemic and renal vasoconstriction caused by exogenously administered endothelin in awake normotensive rats.
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||2 28-2|
|Publication status||Published - 1990|
- Calcium antagonists
- High blood pressure
- Renal blood flow
ASJC Scopus subject areas