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Contributions of α 1 ‐adrenoceptors, α 2 ‐adrenoceptors and P 2x ‐purinoceptors to neurotransmission in several rabbit isolated blood vessels: role of neuronal uptake and autofeedback
Author(s) -
MacDonald A.,
Daly C.J.,
Bulloch J.M.,
McGrath J.C.
Publication year - 1992
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.1476-5381.1992.tb14257.x
Subject(s) - purinergic receptor , rauwolscine , yohimbine , prazosin , endocrinology , medicine , alpha 2 adrenergic receptor , vasoconstriction , biology , chemistry , antagonist , receptor , adenosine
Summary1 . The roles of autofeedback and neuronal uptake in neurotransmission produced by electrical field stimulation in several rabbit isolated blood vessels were examined. 2 . Blocking drugs were used to separate the possible purinergic and noradrenergic contributions to the end organ response: prazosin, antagonist at postjunctional α 1 ‐adrenoceptors; rauwolscine and yohimbine, antagonists at pre‐ and postjunctional α 2 ‐adrenoceptors; α,β‐methylene ATP, desensitizing agent at postjunctional P 2x ‐purinoceptors. In addition to desensitizing postjunctional P 2x ‐purinoceptors, α,β‐methylene ATP potentiated the noradrenergic component of the nerve‐induced responses. 3 . In the presence of an intact neuronal uptake mechanism, the vessels showed different contributions of purinergic (via P 2x ‐purinoceptors) and noradrenergic (via α 1 ‐adrenoceptors and α 2 ‐adrenoceptors) components to the end organ response to nerve stimulation: saphenous artery (approximately equal contributions from P 2x ‐purinoceptors and α 1 ‐adrenoceptors), ileocolic artery (mainly P 2x ‐purinoceptors with a smaller contribution from α 1 ‐adrenoceptors), plantaris vein (mainly α 1 ‐adrenoceptors with a small contribution from α 2 ‐adrenoceptors and P 2x ‐purinoceptors) and saphenous vein (α 1 ‐adrenoceptors). 4 . The presence of α 2 ‐adrenoceptor‐mediated autofeedback could be demonstrated for both purinergic and noradrenergic components of the nerve‐induced responses in the artery preparations. In the veins, potentiation of nerve‐induced responses by α 2 ‐adrenoceptor antagonists could not be studied due to blockade of postjunctional α 2 ‐adrenoceptor‐mediated vasoconstriction. 5 . Blockade of neuronal uptake with cocaine potentiated the noradrenergic component of the nerve‐induced responses. Both α 1 ‐adrenoceptor‐ and α 2 ‐adrenoceptor‐mediated components were potentiated, with a relatively greater potentiation of the α 2 ‐adrenoceptor‐mediated component. In the case of saphenous vein an α 2 ‐adrenoceptor‐mediated component which was previously absent was uncovered. 6 . Blockade of neuronal uptake with cocaine had no effect or reduced the purinergic component of responses, the latter effect presumably due to enhanced α 2 ‐adrenoceptor‐mediated autofeedback. 7 . In the presence of cocaine, nerve‐induced responses in the saphenous vein were biphasic. Rauwolscine potentiated the first phase and inhibited the second phase thus demonstrating effects of pre‐ and postjunctional α 2 ‐adrenoceptor‐mediated activation in the same preparation. 8 . In conclusion, neuronal uptake and autofeedback processes play important and complex interacting parts in determining the relative contributions of α 1 and α 2 ‐adrenoceptors and P 2x ‐purinoceptors in the end organ response to neurotransmission in blood vessels.