Autonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogs

Abstract

In dogs anesthetized with pentobarbital sodium, hilar venous pressure (P(hv)) and secretion were measured from the submandibular gland receiving spontaneous blood flow or vascular perfusion at the normal resting flow rate. Parasympathetic nerve stimulation and ACh-induced secretion increased P(hv) and its pulse pressure; P(hv) also showed an obvious arterial (or perfusion pressure)-like waveform. Vasoactive intestinal polypeptide (VIP) exerted similar effects on P(hv) but produced negligible secretion. Sympathetic nerve stimulation, phenylephrine, and clonidine did not induce secretion and had no significant action on P(hv), whereas isoproterenol provoked secretion and changed P(hv) as with parasympathetic stimulation. Background or superimposed sympathetic nerve stimulation reduced the parasympathetic nerve-induced responses; the sympathetic inhibition was abolished by phentolamine and yohimbine but not by prazosin and propranolol. The results suggest a direct relationship between P(hv) and secretion during parasympathetic salivation: The elevation in P(hv) was primarily independent of the concurrent blood flow response, mediated via muscarinic and peptidergic mechanisms, and related to an opening of arteriovenous anastomoses. Sympathetic inhibition of parasympathetic salivation may be related to prevention of an increased P(hv) exerted primarily via the α2-adrenergic mechanism.