Journal of Applied Physiology, Vol 67, Issue 1 371-376, Copyright © 1989 by American Physiological Society
Analysis of responses to sympathetic nerve stimulation in the feline pulmonary vascular bed
A. L. Hyman and P. J. Kadowitz
Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana 70112.
The adrenergic receptor subtypes mediating the response to sympathetic
nerve stimulation in the pulmonary vascular bed of the cat were
investigated under conditions of controlled blood flow and constant left
atrial pressure. The increase in lobar vascular resistance in response to
sympathetic nerve stimulation was reduced by prazosin and to a lesser
extent by yohimbine, the respective alpha 1- and alpha 2-adrenoceptor
antagonists. Moreover, in animals pretreated with a beta-adrenoceptor
antagonist to prevent an interaction between alpha- and beta
2-adrenoceptors, responses to nerve stimulation were reduced by prazosin,
but yohimbine had no significant effect. On the other hand, in animals
pretreated with a beta-adrenoceptor antagonist, yohimbine had an inhibitory
effect on responses to tyramine and to norepinephrine. Propranolol had no
significant effect on the response to nerve stimulation, whereas ICI
118551, a selective beta 2-adrenoceptor antagonist, enhanced responses to
nerve stimulation and injected norepinephrine. The present data suggest
that neuronally released norepinephrine increases pulmonary vascular
resistance in the cat by acting mainly on alpha 1-adrenoceptors and to a
lesser extent on postjunctional alpha 2-adrenoceptors but that this effect
is counteracted by an action on presynaptic alpha 2-receptors. The present
studies also suggest that neuronally released norepinephrine acts on beta
2-adrenoceptors and that the response to sympathetic nerve stimulation
represents the net effect of the adrenergic transmitter on alpha 1-, alpha
2-, and beta 2-adrenoceptors in the pulmonary vascular bed.
