Vascular relaxing effects of bumetanide

Bumetanide reduced basal tension of resting carotid arteries as well as tonic contraction elicited by 36 mM of KCl, KNO3 and 0.1 mM norepinephrine but had little effect on phasic response to norepinephrine and angiotensin II. Bumetanide was much more active against norepinephrine than KCl, KNO3 and...

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Bibliographic Details
Published in:	Methods and findings in experimental and clinical pharmacology Vol. 11; no. 10; p. 613
Main Authors:	Copello, J, Müller, A, Aquino, S, Villamil, M F
Format:	Journal Article
Language:	English
Published:	Spain 01-10-1989
Subjects:	Angiotensin II - pharmacology Animals Bumetanide - pharmacology Carotid Arteries - drug effects Diuretics - pharmacology Dogs Endothelium, Vascular - drug effects Endothelium, Vascular - physiology In Vitro Techniques Methylene Blue - pharmacology Muscle Relaxation - drug effects Muscle, Smooth, Vascular - drug effects Norepinephrine - pharmacology Potassium - pharmacology Vasodilator Agents
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Summary:	Bumetanide reduced basal tension of resting carotid arteries as well as tonic contraction elicited by 36 mM of KCl, KNO3 and 0.1 mM norepinephrine but had little effect on phasic response to norepinephrine and angiotensin II. Bumetanide was much more active against norepinephrine than KCl, KNO3 and its effect was not reduced by propranolol. These findings establish a distinction between bumetanide and the Ca antagonists, which do not affect basal tension but selectively inhibit potassium (K+) contracture. On the contrary, this compound resembles the nitrocompounds in that vascular relaxation does not require the integrity of endothelium but is abolished by methylene blue. These two common traits support the view that the increased synthesis of cyclic GMP secondary to guanylate cyclase activation may be directly involved in the vasodilating properties of the drug.
ISSN:	0379-0355