Direct visualization of effects of endothelin on the renal microvasculature

R. Loutzenhiser, M. Epstein, K. Hayashi, C. Horton

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136 Citations (Scopus)


The renal microvascular and hemodynamic actions of endothelin were assessed directly in isolated perfused hydronephrotic (HYD) and normal kidneys, respectively. In HYD kidneys endothelin was a potent vasoconstrictor of the afferent arteriole (AA), eliciting a threshold vasoconstrictor response at 0.01 nM (P < 0.05). At 0.1 and 0.3 nM, endothelin reduced AA diameter by 22 ± 6 (P < 0.025) and 41 ± 4% (P < 0.001), respectively. Furthermore, endothelin provoked oscillatory vasomotion in the AA. In contrast, endothelin had less effect on the efferent arteriole (EA), reducing EA diameter by only 7 ± 4 (P > 0.20) and 13 ± 4% (P < 0.05), at 0.1 and 0.3 nM, respectively. In normal kidneys endothelin elicited a long-lasting vasoconstriction with a dose dependency similar to that observed in the AA of HYD kidneys. Furthermore, endothelin reduced glomerular filtration rate (GFR) from 0.58 ± 0.04 to 0.09 ± 0.05 ml·min-1·g-1 (P < 0.001) in this model. Both the AA vasoconstriction and reduction in GFR were completely reversed by nifedipine. These findings indicate that endothelin is a potent renal vasoconstrictor that decreases GFR by a predominant vasoconstriction of the AA. Our observations are consistent with the postulate that endothelin elicits renal vasoconstriction via a mechanism involving dihydropyridine-sensitive calcium channels and that such calcium channels play a prominent role in the activation of the AA.

Original languageEnglish
Pages (from-to)F61-F68
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number1 27-1
Publication statusPublished - 1990 Jan 1


  • Afferent arteriole
  • Calcium antagonists
  • Efferent arteriole
  • Endothelin I
  • Endothelium
  • Renal hemodynamics
  • Resistance arteries
  • Vasomotion

ASJC Scopus subject areas

  • Physiology


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