Multiple factors contribute to acetylcholine-induced renal afferent arteriolar vasodilation during myogenic and norepinephrine-and KCl-induced vasoconstriction: Studies in the isolated perfused hydronephrotic kidney

K. Hayashi, R. Loutzenhiser, M. Epstein, H. Suzuki, T. Saruta

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Acetylcholine (ACh) elicits vasodilation by releasing a number of endothelium-derived relaxing factors (EDRFs). We used the isolated perfused hydronephrotic rat kidney to examine the characteristics of ACh-induced vasodilation of renal afferent arterioles during different types of underlying vasoconstriction. Basal arteriolar tone was increased by either elevating perfusion pressure to 180 mm Hg (myogenic), administering 0.3 μmol/L norepinephrine (NE), or elevating medium potassium concentration to 30 mmol/L (KCl). ACh (10 μmol/L) completely reversed myogenic and NE- induced vasoconstriction and reversed KCl-induced vasoconstriction by 80±5%. However, whereas ACh produced a sustained vasodilation during KCl- and NE- induced vasoconstriction, only a transient reversal of myogenic vasoconstriction was observed, and myogenic tone recovered within 5 to 10 minutes. ACh-induced vasodilation of arterioles preconstricted with KCl was markedly inhibited by either indomethacin (100 μmol/L) or nitro-L-arginine (100 μmol/L) and was completely abolished by pretreatment with both inhibitors. In contrast, indomethacin and nitro-L-arginine had no effect on the transient response to ACh observed during pressure-induced vasoconstriction. In vessels preconstricted with NE, nitro-L-arginine converted the normally sustained response to ACh to a transient vasodilation, which was refractory to both nitric oxide synthase and cyclooxygenase inhibition. Since this component was not observed during KCl-induced vasoconstriction, it may reflect the actions of an, as yet unidentified, endothelium-derived hyperpolarizing factor (EDHF). Our findings thus suggest that prostanoids, nitric oxide, and EDHF all contribute to ACh-induced renal afferent arteriolar vasodilation and that the relative contributions of these individual EDRFs depends on the nature of the underlying renal vascular tone.

Original languageEnglish
Pages (from-to)821-828
Number of pages8
JournalCirculation research
Volume75
Issue number5
DOIs
Publication statusPublished - 1994 Jan 1

Keywords

  • acetylcholine
  • endothelium-derived hyperpolarizing factor
  • nitric oxide
  • prostaglandins
  • renal microcirculation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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