TY - JOUR
T1 - Efficacy of nifedipine to prevent systemic and renal vasoconstrictor effects of endothelin
AU - Madeddu, Paolo
AU - Yang, Xiao Ping
AU - Anania, Vittorio
AU - Troffa, Chiara
AU - Pazzola, Antonio
AU - Soro, Aldo
AU - Manunta, Paolo
AU - Tonolo, Giancarlo
AU - Demontis, Maria Piera
AU - Varoni, Maria Vittoria
AU - Melis, Maria Grazia
AU - Glorioso, Nicola
PY - 1990
Y1 - 1990
N2 - 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.
AB - 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.
KW - Angiotensin
KW - Calcium antagonists
KW - High blood pressure
KW - Norepinephrine
KW - Renal blood flow
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M3 - Article
C2 - 2201205
AN - SCOPUS:0025125949
VL - 259
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 2 28-2
ER -