Inhibition of cardiac vagal action by galanin but not neuropeptide Y in the brush‐tailed possum Trichosurus vulpecula.

Abstract

SUMMARY1. Stimulation of the right cardiac sympathetic nerve for 2 min at 16 Hz in the presence of either ,3-or a-and /3-adrenoceptor blockade evoked attenuation of cardiac vagal action in eight possums: 31-3 + 103 % maximum inhibition of cardiac vagal action on prolonging pulse interval, with a time to half-recovery of 4-9 + 1-1 min.2. Intravenous injection of galanin (2-3 5 nmol kg-') evoked similar inhibition of cardiac vagal action: 41-3 + 41 % maximum inhibition of cardiac vagal action on pulse interval, with a time to half-recovery of 13-4+2-3 min.3.

Galanin and neuropeptide Y reduce cholinergic transmission in the heart of the anaesthetised mouse

“…Following a period of sympathetic stimulation in the mouse, there is a prolonged attenuation of subsequent cardiac vagal activity. Observations in other species suggest this effect to be mediated by multiple transmitters released by the sympathetic nerve during stimulation (Potter, 1985; Revington et al , 1990 ; Courtice et al , 1993 ; Smith‐White et al , 1999 ). While NAd has been shown to inhibitcardiac vagal activity, its effect is very short lasting (Potter, 1988).…”

“…In the Australian possum ( Trichosurus vulpecula ), GAL and not NPY is colocalised with NAd in the thoracic sympathetic ganglia ( Morris et al , 1992 ). In this species exogenous GAL, but not NPY, attenuated cardiac vagal activity, mimicking the effect of sympathetic stimulation and increasing BP ( Courtice et al , 1993 ). While GAL has not been detected as yet in sympathetic nerves in humans, it has been detected in the adrenal medulla and pancreatic tissue, and increased plasma levels of GAL have been reported in humans postexercise ( Legakis et al , 2000 ).…”