Efficacy of nifedipine to prevent systemic and renal vasoconstrictor effects of endothelin

Paolo Madeddu, Xiao Ping Yang, Vittorio Anania, Chiara Troffa, Antonio Pazzola, Aldo Soro, Paolo Manunta, Giancarlo Tonolo, Maria Piera Demontis, Maria Vittoria Varoni, Maria Grazia Melis, Nicola Glorioso

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume259
Issue number2 28-2
Publication statusPublished - 1990

Keywords

  • Angiotensin
  • Calcium antagonists
  • High blood pressure
  • Norepinephrine
  • Renal blood flow

ASJC Scopus subject areas

  • Physiology

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