Abstract
Vasodepressor reactions, characterized by paradoxic bradycardia, were induced in rats when the inferior vena cava was occluded during an infusion of isoproterenol. The effects of alpha-adrenergic receptors and their interaction with beta-adrenergic receptors on the vasodepressor reaction were examined. Inferior vena cava occlusion was performed for 60 s, and the maximum changes in R-R were measured in 44 rats: (i) in control conditions, during phenylephrine (alpha 1-adrenergic agonist), and during a combined infusion of phenylephrine and isoproterenol the R-R shortened significantly (-16.8 +/- 1.4, -24.1 +/- 2.2, and -4.9 +/- 1.2 ms, respectively); (ii) isoproterenol and phentolamine and prazosin (nonselective and selective alpha-adrenergic antagonists) prolonged the R-R paradoxically (+89.2 +/- 9.5, +58.9 +/- 4.1, and +64.4 +/- 10.2 ms, respectively); (iii) atropine and right vagotomy did not affect the phentolamine-induced R-R prolongation (+66.0 +/- 2.4 and +73.8 +/- 13.7 ms, respectively), but it was blocked by left vagotomy (-9.6 +/- 1.1 ms); (iv) propranolol inhibited the prazosin-induced R-R prolongation (-14.3 +/- 2.8 ms,); (v) epinephrine (alpha- and beta-adrenergic agonist) shortened the R-R interval (-9.5 +/- 2.2 ms), but following prazosin, epinephrine induced R-R prolongation (+13.7 +/- 6.0 ms,); (vi) norepinephrine induced R-R prolongation (+21.0 +/- 6.7 ms). It was concluded that (i) paradoxic bradycardia (vasodepressor reaction) dependent on vagal afferents can be induced by reduced venous return in the presence of excess exogenous beta 1-adrenergic stimulation (isoproterenol) or when endogenous alpha-adrenergic tone is antagonized (phentolamine or prazosin); (ii) the reaction can be blocked by alpha 1-adrenergic stimulation; and (iii) epinephrine does not induce paradoxic bradycardia, whereas norepinephrine does, and this may be due to the stronger alpha-stimulating properties of epinephrine.
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