Nitric oxide regulation of ADP-ribosylation of G proteins in hypertension

N. L. Kanagy, J. R. Charpie, R Clinton Webb

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Nitric oxide stimulates endogenous ADP-ribosylation of cytosolic and membrane-bound proteins. Endogenous ADP-ribosyltransferases modify several intracellular proteins including the heterotrimeric GTP-binding proteins (G proteins). ADP-ribosylation of G proteins in vascular smooth muscle leads to increased activation of adenylate cyclase and decreased activation of phospholipase C leading to vasodilation. We hypothesize that in hypertension, chronically depressed endothelium-derived nitric oxide levels lead to decreased ADP-ribosylation of G proteins. This reduced ADP-ribosylation leads to vasoconstriction since activation of the G proteins by agonists is unopposed. Thus, disinhibition of G proteins, mediated by nitric oxide deficit, is responsible for the observed increased sensitivity to vasoconstrictor agonists in hypertension. This novel role for nitric oxide in hypertension will provide a new area of research for antihypertensive therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)159-164
Number of pages6
JournalMedical Hypotheses
Volume44
Issue number3
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

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ASJC Scopus subject areas

  • Medicine(all)
  • Developmental Biology
  • Drug Discovery

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