Effects of ouabain on isolated cerebral and femoral arteries of the cat: a functional and biochemical study

1 This study analyzes the mechanisms involved in the responses to ouabain in cat cerebral and femoral arteries and characterizes the electrogenic Na+ pump present in these vessels. The latter was accomplished by measurement of [3H]‐ouabain binding to arterial membrane fractions, K+‐elicited relaxati...

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Bibliographic Details
Published in:British journal of pharmacology 1988-01, Vol.93 (1), p.43-52
Main Authors: Marín, Jesús, Sánchez‐Ferrer, Carlos F., Salaices, Mercedes
Format: Article
Language:English
Subjects:
Animals
arteries
Binding, Competitive - drug effects
Biological and medical sciences
brain
Cardiotonic agents
Cardiovascular system
Cats
Cerebral Arteries - drug effects
Cerebral Arteries - innervation
Female
Femoral Artery - drug effects
Femoral Artery - innervation
In Vitro Techniques
Isometric Contraction - drug effects
leg
Male
Medical sciences
Muscle Contraction - drug effects
Muscle, Smooth, Vascular - drug effects
Ouabain - pharmacology
Pharmacology. Drug treatments
Phentolamine - pharmacology
Rubidium Radioisotopes
sodium
Sodium-Potassium-Exchanging ATPase - metabolism
Verapamil - pharmacology
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Summary:1 This study analyzes the mechanisms involved in the responses to ouabain in cat cerebral and femoral arteries and characterizes the electrogenic Na+ pump present in these vessels. The latter was accomplished by measurement of [3H]‐ouabain binding to arterial membrane fractions, K+‐elicited relaxation and ouabain‐sensitive 86Rb+ uptake. 2 Ouabain induced transient contraction in cylindrical segments of cerebral arteries. This contraction was reduced by verapamil (3 × 10−6 m) and Ca2+‐removal from the medium but was not modified by phentolamine (3 × 10−6 m) or pretreatment with reserpine. However, the contraction elicited by ouabain in femoral artery segments lasted longer, and was reduced by Ca2+‐omission, phentolamine or reserpine, but remained unaffected by verapamil. 3 The immersion of the arteries in low‐Na+ (25 mm) medium abolished the contraction caused by ouabain. 4 The exposure of the arteries to a K+‐free medium induced a small transient increase in tension, and the subsequent application of K+ (7.5 mm) elicited a marked relaxation. This effect was greater in cerebral than in peripheral arteries, and was suppressed by ouabain (10−4 m). 5 Scatchard analysis of the [3H]‐ouabain binding to arterial membrane fractions suggested a single class of binding sites. The KD values for both kinds of arteries were of similar order, while the Bmax value was greater in cerebral than in femoral arteries. 6 Total and ouabain‐sensitive 86Rb+ uptakes were greater in cerebral than in femoral vessels. 7 These results indicate that: (1) ouabain‐induced contraction of cerebral arteries is due to a direct effect on vascular smooth muscle cells, while in femoral arteries it is due to noradrenaline release from adrenergic nerve terminals; and (2) the electrogenic Na+ pump activity is greater in cerebral than in peripheral arteries.
ISSN:0007-1188
1476-5381
DOI:10.1111/j.1476-5381.1988.tb11403.x