Article date: March 1991
By: Clive N. May, Catherine J. Whitehead, Christopher J. Mathias, in Volume 102, Issue 3, pages 639-644
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.
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 Paco2 and fall in Pao2; these effects were reversed by intravenous (i.v.) naloxone (300 nmol kg−1).
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.
After i.c. β‐endorphin, MAP, HR and plasma catecholamines were not significantly altered but there was a similar degree of respiratory depression.
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).
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.
A role for β‐endorphin in the central hypotensive action of α2‐adrenoceptor agonists was opposed by finding that opioid receptor antagonism with naloxone did not block the effects of clonidine.
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.
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 Paco2 and fall in Pao2; these effects were reversed by intravenous (i.v.) naloxone (300 nmol kg−1).
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.
After i.c. β‐endorphin, MAP, HR and plasma catecholamines were not significantly altered but there was a similar degree of respiratory depression.
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).
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.
A role for β‐endorphin in the central hypotensive action of α2‐adrenoceptor agonists was opposed by finding that opioid receptor antagonism with naloxone did not block the effects of clonidine.
DOI: 10.1111/j.1476-5381.1991.tb12226.x
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