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REVERSAL OF ADRENALINE‐INDUCED CONTRACTION IN THE RABBIT PULMONARY ARTERY BY CLONIDINE
Author(s) -
Katsuragi T.,
Mori R.,
Su C.,
Furukawa T.
Publication year - 1984
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1984.tb00264.x
Subject(s) - clonidine , prazosin , yohimbine , phentolamine , contraction (grammar) , chemistry , phenylephrine , medicine , endocrinology , antagonist , propranolol , receptor , blood pressure
SUMMARY 1. Characterization of clonidine which reversed the adrenaline‐induced contractions was assessed using the rabbit pulmonary arterial segment. 2. Clonidine in high concentrations (10 −5 ‐10 −4 mol/l) contracted this vascular tissue. Nevertheless, an adrenaline (3 × 10 −6 mol/l)‐induced contraction, which can be markedly depressed by phentolamine, was reversed to relaxation by pre‐addition of 3 × 10 −5 mol/l clonidine. This reversal was abolished by mol/l propranolol, a β‐adrenoceptor antagonist. 3. The cumulative concentration‐contraction curve for adrenaline was shifted to the right by 10 −5 mol/l clonidine without further alteration at 10 −4 mol/l, suggesting a partial agonistic feature of clonidine for α‐adrenoceptors. 4. Contractions evoked by 5 × 10 −5 mol/l clonidine alone were effectively reduced by prazosin (IC 50 = 1.7 × 10 −7 mol/l) or yohimbine, (IC 50 = 3.3 × 10 −5 mol/l) and those by phenylephrine (10 −5 mol/l) were suppressed as well (prazosin, IC 50 = 3.4 × 10 −8 mol/l; yohimbine, IC 50 = 5.0 × 10 −6 mol/l). However, the depolarization‐induced contractions with 30 mmol/l KCl were virtually unaltered by both antagonists. 5. These results suggest that the reversal action of clonidine on the adrenaline‐induced contraction is primarily mediated by a partial agonistic property for postsynaptic α 1 ‐adrenoceptors.