Autonomic regulation of somatostatin release: studies with primary cultures of canine fundic mucosal cells

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Abstract
Using a newly developed system for culturing canine fundic mucosal cells, the regulation of somatostatin-like immunoreactivity (SLI) secretion by cholinergic and adrenergic transmitters was studied. Enzyme-dispersed canine fundic mucosa cells were enriched in SLI content by counterflow elutriation and cultured on collagen for 42 h. Epinephrine alone and in combination with gastrin stimulated SLI secretion in a dose-dependent fashion. Propranolol did not alter the response to dibutyryl cAMP or gastrin but produced a parallel, rightward shift of the epinephrine dose-response curve with the Kd determined to be 14 nM by nonlinear curve fitting. Phentolamine, an .alpha.-adrenergic antagonist, enhanced SLI secretion in response to epinephrine, an effect reversed by the .alpha.1-agonist methoxamine but not by the .alpha.2-agonist clonidine. Neither methoxamine nor clonidine alone inhibited the response to the .beta.-selective adrenergic agonist isoproterenol; thus, the existence of an adrenergic .alpha.1-inhibitory receptor remained uncertain. Carbachol noncompetitively inhibited SLI secretion stimulated by gastrin, epinephrine and dibutyryl cAMP. Atropine produced a parallel rightward shift of the carbachol dose-response curve (Kd = 0.4 nM). Pirenzepine also inhibited the effects of carbachol (Kd= 35 nM). SLI-containing cells in the canine fundic mucosa apparently possess stimulatory .beta.-adrenergic receptors and inhibitory muscarinic receptors.