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Gerkens, J.F. et al.

Chemical renal medullectomy prevents frusemide-induced inhibition of sympathetic vasoconstriction in the in situ blood perfused rat mesentery.

The mesentery of anaesthetized rats was perfused in situ at a constant rate, via the cannulated superior mesenteric artery, with blood drawn from a cannulated carotid artery. Increases in perfusion pressure were produced by peri-arterial electrical stimulation of the mesenteric sympathetic nerves at 3, 6 and 10 Hz before and after the intravenous administration of frusemide 5 mg/kg. Loss of solutes and volume as a result of frusemide-induced diuresis was prevented by a urinary bladder-venous shunt. In control animals the vasoconstrictor responses to mesenteric nerve stimulation were significantly reduced after frusemide administration. However, in animals pretreated 4 weeks previously with bromethylamine (BEA) 200 mg/kg i.p., frusemide had no effect on vasoconstrictor responses. Chemical papillectomy with BEA has been shown by others to prevent the antihypertensive effects attributed to the non-prostanoid lipids produced by the interstitial cells of the renal medulla. Our data suggest that the vasoconstrictor-inhibiting effect of frusemide may be mediated by the release of renomedullary lipids.[1]

References

Chemical renal medullectomy prevents frusemide-induced inhibition of sympathetic vasoconstriction in the in situ blood perfused rat mesentery. Gerkens, J.F., Armsworth, S.J., Bhagwandeen, S.B., Smith, A.J. J. Hypertens. (1987) [Pubmed]

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