Role of XXXX in the renal and systemic vasodilatory responses to platelet-activating factor in the @entity35 , in vivo.

@entity101 @entity842 @entity35 @entity5567 @entity551
BACKGROUND/AIM: Chemical mediator(s) involved in the renal vasodilatory and systemic @entity551 effects of platelet-activating factor ( @entity5567 ) remain unresolved. Because @entity842 (NO) and @entity5567 have many similar cardiovascular actions, we examined whether endogenous NO contributes to the renal and systemic actions of @entity5567 . METHODS: @entity5567 was administered into the renal arterial or systemic venous circulation of anesthetized @entity35 . The change in renal blood flow (RBF) and/or mean arterial blood pressure (MAP) was recorded in the absence and presence of NO synthase inhibition. RESULTS: Transient exposure of the renal vacsular bed to intrarenal @entity5567 boluses (1-10 ng kg(-1)) resulted in an immediate increase in RBF that was partially inhibited by the intrarenal administration of a NO synthase inhibitor, whereas the ensuing rapid fall in MAP was unaffected by NO synthase blockade. A sustained exposure to intrarenal @entity5567 infusion (2.5 ng min(-1) kg(-1)) in intrarenal NO synthase inhibitor-treated @entity35 ( @entity101 with vasoconstricted kidneys) had no effect on RBF and MAP, which was in contrast to the increase in RBF and modest fall in MAP in control intrarenal vasopressin-treated @entity35 ( @entity101 with vasoconstricted kidneys). To dissociate the influence of systemic @entity551 on the RBF response, @entity35 kidneys were denervated and MAP elevated by a pressor agent whilst maintaining renal arterial blood pressure constant. Subsequent intrarenal @entity5567 infusion at 2.5 and 10 ng min(-1) kg(-1) resulted in a substantial rise in RBF and modest fall in MAP, responses that were abolished by intrarenal NO synthase inhibition at the lower intrarenal @entity5567 infusion or abolished/attenuated at the higher intrarenal @entity5567 infusion. Additional experiments administered drugs intravenously to exclude the possibility that the modified MAP response by NO synthase inhibition was related to the drugs being administered into the kidney. Intravenous @entity5567 boluses (0.1-1 microg kg(-1)) resulted in a transient fall in MAP that was independent of the NO pathway, whereas the systemic @entity551 induced by intravenous @entity5567 infusion (10 ng min(-1) kg(-1)) was greatly attenuated by NO synthase inhibition. CONCLUSION: NO has a major role in mediating the renal and peripheral vasodilatory responses induced by a sustained exposure to @entity5567 in the @entity35 , whereas NO's overall contribution was less or absent during transient @entity5567 exposure.
