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Hypothesis-generating for rat gastric autonomic control; leaves open human translation and clinical relevance.
The effects of autonomic nerve stimulation on rat gastric blood flow (GBF) were studied using a cross thermocouple method. Stimulation of the periarterial nerve bundles along the left gastric artery produced a decrease in GBF which was antagonized by phenoxybenzamine (0.05 mg kg-1 i.v.), but not by propranolol (1 mg kg-1 i.v.). Stimulation of the vagus nerves elicited an increase in GBF, within a latency of 20 s, which was not apparently affected by atropine (0.15 and 1.5 mg kg-1 i.v.) but was completely blocked by hexamethonium (10 mg kg-1 i.v.). The GBF increase due to acetylcholine (0.25 micrograms rat-1 i.a.), was markedly blocked by atropine (0.15 mg kg-1 i.v.). Vagal stimulation also produced both the cholinergic excitation and non-cholinergic inhibition of gastric motility. The vagally induced GBF increase was little affected by any pretreatment with phentolamine, propranolol, indomethacin or aprotinin. These results suggest that sympathetic nerve stimulation creases GBF through alpha-adrenoceptors and parasympathetic nerve stimulation increases GBF through a non-cholinergic mechanism in rats and that the GBF increase may result from a primary dilator effect of vagal stimulation on the blood vessels because of the immediate initiation of the response.
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Yano et al. (1983) studied this question.
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