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The pressor response to central administration of β‐endorphin results from a centrally mediated increase in noradrenaline release and adrenaline secretion
Author(s) -
May Clive N.,
Whitehead Catherine J.,
Mathias Christopher J.
Publication year - 1991
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.1476-5381.1991.tb12226.x
Subject(s) - yohimbine , medicine , endocrinology , (+) naloxone , prazosin , opioid , vasoconstriction , opioid peptide , clonidine , chemistry , receptor , antagonist
1 The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) administration of β‐endorphin (0.01, 0.1 and 1.0 nmol kg −1 ) were examined in conscious rabbits. 2 After i.c.v. β‐endorphin, mean arterial pressure (MAP) increased, heart rate (HR) fell, plasma noradrenaline, adrenaline and glucose increased and there was a rise in P aco 2 and fall in P ao 2 ; these effects were reversed by intravenous (i.v.) naloxone (300 nmol kg −1 ). 3 A combination of prazosin (2 mg kg −1 ) and yohimbine (1 mg kg −1 ), given i.v., prevented the rise in MAP induced by i.c.v. β‐endorphin. 4 After i.c. β‐endorphin, MAP, HR and plasma catecholamines were not significantly altered but there was a similar degree of respiratory depression. 5 Clonidine (1.0 μg kg −1 , i.c.) reduced MAP and HR; these effects were not blocked by i.v. naloxone (6 μmol kg −1 ). 6 These results demonstrate that β‐endorphin acts centrally, probably mainly on periventricular μ‐opioid receptors, to increase adrenaline secretion and sympathetic nerve activity leading to α‐adrenoceptor‐mediated vasoconstriction. The respiratory depression is probably mediated by brainstem μ‐receptors. 7 A role for β‐endorphin in the central hypotensive action of α 2 ‐adrenoceptor agonists was opposed by finding that opioid receptor antagonism with naloxone did not block the effects of clonidine.