Sodium intake modulates renal vascular reactivity to endothelin-1 in Dahl rats

Clin Exp Pharmacol Physiol. 1990 Feb;17(2):121-8. doi: 10.1111/j.1440-1681.1990.tb01294.x.

Abstract

1. The systemic and renal haemodynamic responses to endothelin-1 (ET1) were evaluated and compared to Angiotensin II (AII) in anaesthetized Dahl salt-sensitive (DS) and salt-resistant (DR) rats on either low (0.1% NaCl in diet) or high (8% NaCl in diet) salt intake. 2. Baseline mean arterial pressure on low salt diet was similar in both strains, while on high salt diet it was 73 +/- 4 mmHg in DR rats and 119 +/- 8 mmHg in DS rats (P less than 0.05). Baseline renal blood flow (RBF) and renal vascular resistance (RVR) were similar in all groups. 3. AII in bolus injection induced a short, dose-dependent increase in blood pressure and renal vascular resistance and a fall in renal blood flow. The maximal pressure increase was significantly greater in DS rats on high salt diet than that in each of the other groups (P less than 0.05). The fall in renal blood flow and the increase in renal vascular resistance were attenuated in both strains on low salt diet. 4. ET1 induced an initial decrease followed by a prolonged increase in blood pressure; both phases were similar in all groups. However, renal vascular reactivity to ET1 was markedly modulated by salt intake. On low salt diet, following a bolus injection of ET1 (1 nmol/kg), RBF decreased by 34% in DR and by 20% in DS rats, while on high salt diet RBF decreased by 76% in DR and by 80% in DS rats (P less than 0.05 high vs low salt).(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Comparative Study

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Blood Pressure / drug effects
  • Dose-Response Relationship, Drug
  • Endothelins
  • Heart Rate / drug effects
  • Male
  • Peptides / pharmacology*
  • Rats
  • Renal Circulation / drug effects*
  • Sodium Chloride / pharmacology*
  • Sodium Chloride / urine
  • Vascular Resistance / drug effects*

Substances

  • Endothelins
  • Peptides
  • Angiotensin II
  • Sodium Chloride