Abstract:
:In isolated rat tail arteries perfused with Krebs-Henseleit solution, ouabain, in concentrations of less than 10(-5) M, caused a concentration-dependent, noncompetitive inhibition of the vasoconstrictor response to phenylephrine. Concentrations of 10(-8) and 10(-6) M caused 30 and 61% inhibition, respectively. The inhibition was gradual in onset, with a maximal effect at 45 min. In concentrations greater than 10(-5) M, ouabain caused a parallel shift to the left of the phenylephrine dose-response curve, indicating potentiation. The potentiation was rapid in onset (within 1 min), and was approximately 1.4-fold. The cutoff point between inhibition and potentiation of vasoconstrictors occurred at a ouabain concentration of 10(-5) M. Ouabain-induced potentiation was nonspecific in regard to the vasoconstrictor used. Phenylephrine, clonidine, and serotonin were each potentiated. Potentiation probably resulted from a reduction in the smooth muscle membrane potential as a consequence of inhibition of Na-K ATPase. The mechanism of the inhibitory effect of ouabain on vasoconstrictors was not resolved but may operate via stimulation of Na-K ATPase. The results are consistent with a "partial agonist" action of ouabain on Na-K ATPase.
journal_name
J Cardiovasc Pharmacoljournal_title
Journal of cardiovascular pharmacologyauthors
Armsworth SJ,Marwood JF,Stokes GSdoi
10.1097/00005344-198507000-00013subject
Has Abstractpub_date
1985-07-01 00:00:00pages
694-9issue
4eissn
0160-2446issn
1533-4023journal_volume
7pub_type
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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