The effect of opiates on arterial baroreceptor reflex function in the rabbit

The contribution of exogenous and endogenous opioid peptides to the central modulation of the baroreceptor reflex was investigated in rabbits. Baroreceptor sensitivity was assessed in pentobarbitone anaesthetised animals by measuring heart period in response to rises in arterial pressure after bolus intravenous injections of phenylephrine and falls induced by intravenous sodium nitroprusside and controlled haemorrhage. The slope of the linear relationship between arterial pressure and heart period was used as an index of baroreflex sensitivity. Thirty minutes after the intracisternal administration of 50 microgram/kg RX783016 (a mu-opiate receptor agonist) baroreceptor sensitivity was reduced to all three methods of blood pressure manipulation. Ketazocine (50 microgram/kg) a kappa-opiate agonist and [D-Ala2, D-Leu5] enkephalin (1 microgram/kg) a delta-opiate agonist, 15 min after intracisternal injection caused an increase in baroreflex sensitivity in response to a rise in pressure and a reduction in response to a fall. Intravenous injection of naloxone (80 microgram/kg) caused an increase in varoreflex gain. However, a higher dose (200 microgram/kg) was required to attenuate the effects of RX783016 and [D-Ala2, D-Leu5] enkephalin but not ketazocine. No change in baseline arterial pressure or heart rate occurred after the opiates or naloxone. It appears that exogenous and endogenous opiates modify baroreceptor reflex function, through a mechanism which involves central opiate receptors of the mu- and kappa-types.