The effect of cold stress on the modulation of vascular adrenergic transmission by acetylcholine Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/pr76f695s

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  • The effect of acetylcholine on vascular adrenergic neuroeffector transmission was investigated. Caudal arteries of rats were isolated and their responses to electrical stimulation of the adrenergic nerves and/or acetylcholine were monitored. Acetylcholine had no effect on the basal perfusion pressure or the vascular response to norepinephrine in arteries from non-stressed rats. In arteries from non-stressed animals acetylcholine caused a dose dependent inhibition of the response to electrical stimulation and the inhibition was blocked by atropine. The conclusion from the data is that acetylcholine inhibits the vascular response to electrical stimulation in the caudal artery of the rat via an action on presynaptic muscarinic receptors. Rats subjected to five days of cold stress at 2.5°C show a significant increase in- sympathetic nervous system activity in the tail artery as measured by a three-fold elevation in the tyrosine hydroxylase activity. Caudal arteries from cold-stressed rats showed no significant difference in their response to acetylcholine administered by itself or to exogenous norepinephrine when compared to the arteries from the non-stressed group. Following cold stress, no significant difference was measured in the effect of acetylcholine on the arteries' response to exogenous norepinephrine when compared to the non-stress group. Likewise there was no significant difference between arteries of the two treatment groups in the ability of atropine to block the response to electrical stimulation. It can be concluded that the response of the postsynaptic effector unit to norepinephrine is not altered by cold stress, and that acetylcholine does not effect this response. It is also concluded that acetylcholine inhibits the vascular response of arteries from cold-stressed rats to electrical stimulation via presynaptic muscarinic receptors. When arteries were electrically stimulated at a constant frequency and the inhibition of the response by acetylcholine measured, the response in arteries from cold-stressed rats was inhibited to a significantly greater degree when compared to arteries from non-stressed rats. Regression analysis showed the log-dose inhibition curve of arteries from the cold-stressed rats to be parallel to the curve of the non-stressed arteries and shifted to the left. Arteries were also stimulated with electrical stimulation at variable frequencies and the vascular response inhibited with a constant concentration of acetylcholine. Acetylcholine was found to inhibit the response of the arteries from cold-stressed rats significantly more than the arteries from non-stressed rats. Regression analysis again showed a parallel shift in the dose response curve of the arteries from coldstressed rats. It can be concluded from the data that the presynaptic muscarinic receptors have become supersensitive in the presence of increased sympathetic nerve activity.
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