Abstract

In the Nucleus Ambiguus (NA) mu-receptors increased mean arterial pressure (MAP) and heart rate (HR) and kappa-receptors decreased MAP without altering HR. Mu-receptors in the Dorsal Motor Nucleus of the Vagus (DMV) increased MAP without changing HR whereas kappa-receptors in the DMV decreased HR without changing MAP. The pathways which mediate these responses were studied in anesthetized, artificially ventilated rats. Transection of the spinal cord at the C1 segment blocked the pressor response and tachycardia elicited following microinjection of a mu-agonist into the NA. The depressor response elicited by a kappa-agonist was not changed. Complete attenuation of the kappa response was produced by combining spinal transection with bilateral vagotomy. The pressor response produced following microinjection of a mu-agonist into the DMV was attenuated by pretreatment with the sympathetic blocking drug guanethidine. Atropine methyl nitrate pretreatment blocked the bradycardia elicited by a kappa-agonist and revealed an underlying tachycardic response to the mu-agonist. These data show that mu- and kappa-receptors in the NA and DMV modulate cardiovascular activity by selective modulation of sympathetic and parasympathetic pathways.

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