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Effects of glibenclamide on systemic and splanchnic haemodynamics in conscious rats
Author(s) -
Moreau Richard,
Komeichi Hirokazu,
Kirstetter Philippe,
Yang Song,
AupetitFaisant Brigitte,
Cailmail Stéphane,
Lebrec Didier
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb13124.x
Subject(s) - glibenclamide , vasoconstriction , medicine , vasodilation , splanchnic , vascular resistance , diazoxide , nicardipine , cromakalim , endocrinology , anesthesia , hemodynamics , blood pressure , diabetes mellitus , insulin
1 The effects of the sulphonylurea, glibenclamide (20 mg kg −1 , i.v.), at a dose that blocks vascular potassium channels, on systemic and splanchnic haemodynamics (radioactive microspheres) were studied in conscious rats. 2 Glibenclamide significantly decreased cardiac index and hepatic artery blood flow while it significantly increased vascular resistance in systemic, portal and hepatic arterial territories. 3 In rats with suppressed cardiovascular reflexes, glibenclamide induced vasoconstriction in systemic, portal and hepatic arterial territories. 4 Intracerebroventricular administration of glibenclamide did not alter systemic or regional vascular tone. 5 Glibenclamide blunted the vasodilator effect of the potassium channel opener, diazoxide but not that of the L‐type calcium channel blocker, nicardipine. 6 Another sulphonylurea, glipizide (20 mg kg −1 , i.v.), induced significant systemic and splanchnic vasoconstriction. 7 Thus, the glibenclamide‐induced blockade of vascular potassium channels caused a vasoconstriction in the systemic and splanchnic vascular beds. In these territories, therefore, the opening of glibenclamide‐sensitive potassium channels might be responsible for a basal vasodilator tone.