Renal effects of low dose prazosin in patients with congestive heart failure

Eur Heart J. 1993 Sep;14(9):1245-52. doi: 10.1093/eurheartj/14.9.1245.


Activation of the sympathetic nervous system may contribute to the renal vasoconstriction and sodium retention seen in congestive heart failure. Previous studies in congestive heart failure patients employing large doses of prazosin that lowered systemic blood pressure have been generally disappointing. The renal haemodynamic and segmental tubular effects of low non-depressor doses of prazosin (0.25 mg and 0.50 mg) were examined in eight female patients with mild to moderate congestive heart failure. Segmental tubular function was assessed by the lithium clearance method. Compared to placebo, prazosin caused a significant increase in urinary sodium excretion (from 56 +/- 7 to 92 +/- 7 mumol.min-1, P < 0.01), paralleled by significant increases in fractional excretion of sodium and lithium. Glomerular filtration rate and effective renal plasma flow were not altered by prazosin. Prazosin pre-treatment did not alter any of the renal responses to frusemide treatment (mean dose 85 +/- 14 mg). This study demonstrates that low non-depressor doses of prazosin have a clear natriuretic effect in congestive heart failure patients, which is predominantly established by interference with tubular reabsorption.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Female
  • Furosemide / pharmacology
  • Glomerular Filtration Rate / drug effects
  • Heart Failure / drug therapy
  • Heart Failure / physiopathology*
  • Heart Failure / urine
  • Hemodynamics / drug effects
  • Humans
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / physiopathology
  • Middle Aged
  • Prazosin / administration & dosage
  • Prazosin / pharmacology*
  • Prazosin / therapeutic use
  • Single-Blind Method
  • Sodium / urine
  • Vascular Resistance / drug effects


  • Furosemide
  • Sodium
  • Prazosin