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Glucocorticoids decrease endothelin-A- and -B-receptor expression in the kidney.

A Villeneuve1, S Gignac, P H Provencher

  • 1Department of Medicine, Faculty of Medicine, Université de Sherbrooke, Quebec, Canada.

Journal of Cardiovascular Pharmacology
|November 15, 2000
PubMed
Summary
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Glucocorticoids like dexamethasone increase blood pressure by reducing kidney endothelin receptors (ET(A) and ET(B)). This study shows dexamethasone affects these receptors, not preproendothelin-1 (PPET-1) expression, in hypertensive rats.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Glucocorticoids influence circulatory homeostasis and can cause hypertension.
  • Excess glucocorticoids alter gene expression related to blood pressure, including preproendothelin-1 (PPET-1) and endothelin receptors (ET(A), ET(B)).
  • Both glucocorticoids and endothelin-1 (ET-1) impact kidney function, vascular resistance, and sodium balance.

Purpose of the Study:

  • To investigate the effects of glucocorticoids on renal PPET-1, ET(A), and ET(B) receptor expression in a rat model of glucocorticoid-induced hypertension.
  • To determine the relationship between dexamethasone administration, blood pressure, and the expression of key genes in the kidney.

Main Methods:

  • Wistar rats were administered dexamethasone (a glucocorticoid agonist) in drinking water for 1 or 5 days.

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  • Systolic blood pressure (SBP) was measured.
  • Quantitative analysis of ET(A) and ET(B) receptor mRNA levels and PPET-1 mRNA levels in kidney tissue was performed.

    • Main Results:

    • Dexamethasone administration significantly increased SBP in rats, from 120 mmHg to 139 mmHg (1 day) and 150 mmHg (5 days).
    • Renal ET(A) and ET(B) receptor mRNA levels decreased significantly after 1 day (to 83% and 80% of control, respectively) and further declined after 5 days (to 67% and 65% of control, respectively).
    • Kidney PPET-1 expression remained unaffected by dexamethasone treatment.

    Conclusions:

    • Glucocorticoid administration, exemplified by dexamethasone, leads to hypertension in rats.
    • Dexamethasone treatment downregulates renal endothelin receptor expression (ET(A) and ET(B)) without altering PPET-1 expression.
    • These findings suggest that renal endothelin receptors play a role in the hypertensive effects of glucocorticoids.