The study demonstrates that renal vasoconstriction associated with systemic NSAIDs (indomethacin/meclofenamate) in dogs is driven by the withdrawal of endogenous prostaglandin vasodilator activity rather than unopposed angiotensin II or alpha-adrenergic action.
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Animal data preclude changing NSAID renal risk assessment in patients; leaves open prostaglandin-sympathetic interactions for human validation.
In the anesthetized dog, neither renal angiotensin II blockade nor systemic administration of meclofenemate altered the renal vascular response to renal nerve stimulation or exogenous norepinephrine. Systemic administration of indomethacin enhanced the renal vascular response to exogenous norepinephrine but not to renal nerve stimulation. Renal blockade to angiotensin II, alone or combined with renal α-adrenergic receptor blockade produced by phenoxy-benzamine did not affect the renal vasoconstrictor response to systemically administered indomethacin or meclofenemate. These data demonstrate that neither endogenous circulating angiotensin II nor prostaglandins significantly alter the effects of the sympathetic nervous system on the canine renal vascular bed. The renal vasoconstriction associated with systemic indomethacin or meclofene-mate administration is not due to unopposed angiotensin II or α-adrenergic agonist vasoconstrictor action but rather to the withdrawal of endogenous prostaglandin vasodilator activity.
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Zambraski et al. (1979) studied this question.
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