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Purinoceptors in the pulmonary circulation of the rat and their role in hypoxic vasoconstriction
Author(s) -
McCormack D.G.,
Barnes P.J.,
Evans T.W.
Publication year - 1989
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.1476-5381.1989.tb12606.x
Subject(s) - vasoconstriction , hypoxic pulmonary vasoconstriction , purinergic receptor , vasodilation , medicine , endocrinology , angiotensin ii , vasoconstrictor agents , desensitization (medicine) , receptor , stimulation , chemistry , anesthesia
1 P 2 ‐purinoceptors have been characterized in the systemic circulation of a variety of species but little is known about their nature in the pulmonary vasculature. 2 In the isolated, blood perfused and ventilated lung of the rat the P 2x selective analogues α,β‐methylene ATP(α,β‐meATP) (25 μg) and β,γ‐methylene ATP (400 μg) caused a rise in pulmonary artery pressure (127 ± 32% and 110 ± 23% increase respectively, n = 6), demonstrating the existence of vasoconstrictor P 2 receptors in the pulmonary circulation. 3 Repeated boluses of α,β‐meATP resulted in complete desensitization of the constrictor response to β,γ‐meATP, but a small vasodilator response remained indicating unopposed stimulation of P 2y receptors. The desensitization by α,β‐meATP had no effect on angiotensin II‐induced vasoconstriction. 4 After desensitization of the vasoconstrictor P 2 receptors with α,β‐meATP, hypoxic pulmonary vasoconstriction remained intact, indicating that these receptors are not involved in this response.