INHIBITORY ACTIONS OF METHIONINE‐ENKEPHALIN AND MORPHINE ON THE CAT CAROTID CHEMORECEPTORS

E-ISSN： 1476-5381|71|1|297-305

ISSN： 0007-1188

Source： BRITISH JOURNAL OF PHARMACOLOGY (ELECTRONIC), Vol.71, Iss.1, 1980-01, pp. : 297-305

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

1The effects of intracarotid injections of methionine‐enkephalin (Met‐enkephalin) and morphine on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve have been studied in cats anaesthetized with pentobarbitone.2Met‐enkephalin caused a rapid, powerful, inhibition of spontaneous chemoreceptor discharge, the intensity and duration of which was dose‐dependent.3Morphine was a less potent inhibitor of spontaneous chemoreceptor discharge, and the inhibition it evoked was rather variable and tended to be biphasic. Low doses of morphine caused a slight increase in discharge.4Naloxone (0.2 mg i.c.) slightly increased spontaneous discharge, greatly reduced the chemo‐inhibition caused by morphine, and reduced the inhibitory effect of Met‐enkephalin. A higher dose of naloxone (0.8 mg) caused a substantial reduction of the Met‐enkephalin effect.5Chemo‐excitation evoked by intracarotid injections of acetylcholine, CO2‐saturated Locke solution, and sodium cyanide were only slightly and somewhat variably reduced following injections of Met‐enkephalin, whereas the inhibitory effect of dopamine was potentiated. Following morphine administration, responses to acetylcholine and sodium cyanide were reduced slightly, whereas those to CO2 and dopamine were potentiated.6Responses to acetylcholine and CO2 were slightly potentiated during infusion of Met‐enkephalin (50 μg/min, i.c.) and the response to sodium cyanide was slightly reduced.7It is concluded that naloxone‐sensitive opiate receptors are present in the cat carotid body; when activated they cause inhibition of spontaneous chemoreceptor discharge. The physiological role of these receptors and the identity of any endogenous ligand remains to be established.