Selective inhibition of vasoconstrictor responses by platelet-activating factor in rat kidney

R. K. Handa, J. W. Strandhoy, V. M. Buckalew

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We examined the effect of platelet-activating factor (PAF) on renal vascular reactivity in the pentobarbital sodium-anesthetized male Wistar rat. Intrarenal infusion of C16-PAF at hypotensive (2.5 ng·min-1·kg-1) or nonhypotensive (0.5 ng·min-1·kg-1) doses caused renal vasodilation and dose dependently antagonized the renal vasoconstrictor responses of intrarenal boluses of angiotensin II (ANG II) > norepinephrine (NE) > vasopressin (AVP). PAF infusion at the high dose did not alter non-receptor-mediated renal vasoconstriction induced by intrarenal KCl injection. The inhibitory effect of PAF on agonist-induced renal vasoconstriction was accentuated by eicosanoid synthesis inhibition (indomethacin or dexamethasone), unaffected by dopamine-receptor blockade (haloperidol) but was totally abolished by PAF receptor antagonism (L-659,989). In contrast, intrarenal infusion of a calcium channel antagonist (nimodipine) or an intracellular calcium channel antagonist (TMB-8) equally inhibited the renal vasoconstrictor responses of ANG II, NE, and AVP. Thus PAF can cause renal vasodilation in the rat kidney and dose-dependently antagonizes the renal vasoconstrictor responses of ANG II > NE > AVP. The inhibitory effect of PAF on renal vasoconstrictor responses is mediated by PAF receptors and does not appear to be due to a nonspecific membrane effect, reduction in calcium mobilization, or the release of vasodilatory eicosanoids or dopamine.

Original languageEnglish (US)
Pages (from-to)F108-F116
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number1 30-1
StatePublished - Sep 17 1991



  • Angiotensin II
  • Blood pressure
  • Dopamine
  • Eicosanoids
  • Nimodipine
  • Norepinephrine
  • Platelet-activating factor receptor antagonist
  • Renal blood flow
  • TMB-8
  • Vasodilation
  • Vasopressin

ASJC Scopus subject areas

  • Physiology

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