Effect of intraantral and intrabulbar pH on somatostatin-like immunoreactivity in peripheral venous blood of conscious dogs. The possible function of somatostatin as an inhibitory hormone of gastric acid secretion and its possible identity with bulbogastrone and antral chalone.

Abstract

The aim of the present study was to investigate whether circulating somatostatin takes part in the inhibition of gastric acid secretion induced by acidification of the antrum and the duodenal bulb. Dogs provided with chronic pouches of the antrum or the duodenal bulb, and with Pavlov pouches were used in the study. Peripheral venous somatostatin levels rose on the average to ˜36±15 pmol/1 and 20±3 pmol/1 during perfusion of the antral or bulbar pouches with 0.1 M HC1 respectively. A slight increase was also obtained on antral perfusion with solutions of pH 2.2–3 and on bulbar perfusion with solutions of pH 2.2, whereas peripheral somatostatin levels remained unchanged, when the pouches were exposed to solutions of higher pH. The increase of plasma somatostatin levels coincided in time with the release of somatostatin into the lumen of the antrum and of the duodenal bulb, which showed the same pH dependency. Also plasma gastrin levels rose during perfusion of the pouches with 0.1 M HCI, this was especially the case during perfusion of the antral pouches. Perfusion of bulbar pouches, but not of antral pouches with 0.1 M HC1 inhibited the pentagastrin (2 μg/kg/h) stimulated gastric acid secretions. Infusions of somatostatin (0.15, 0.3 and 0.6 nmol/kg/h) caused plasma somatostatin levels ˜0, 0–20 and ˜50 pmol/1 respectively. Infusions of somatostatin (0.3‐1.2 nmol/kg/h) inhibited pentagastrin stimulated (2 μg/kg/h) gastric acid secretion and 0.15 nmol/kg/h inhibited the acid secretion induced by pentagastrin (1 μg/kg/h). Thus infusions of somatostatin which inhibited pentagastrin induced acid secretion gave rise ot plasma somatostatin levels of comparable size ˜(0–50 pmol/1) to those induced by acidification of the antrum or the duodenal bulb ˜(36 and 20 pmol/1). We therefore suggest that endogenously released somatostatin may account for the inhibition of gastric acid secretion observed during acidification of the duodenal bulb, thus corresponding to the postulated hormone bulbogastrone. The existence of similar inhibitory substance of antral origin (i. e. the antral chalone) has been proposed. We also suggest that this substance corresponds to somatostatin, despite the fact that it is difficult to inhibit pentagastrin‐induced gastric acid secretion by acidification of the antrum. It is suggested that the inhibitory effect on gastric acid secretion exerted by somatostatin released from the antrum might be masked under the present experimental conditions. Thus, gastrin and perhaps also other peptides, which stimulate acid secretion, are also released by antral acidification and they might in part counteract the depressant effect on acid secretion induced by somatostatin. Furthermore, since the antral pouches were innervated, vagovagal reflexes induced by antral acidification might also influence the rate of acid secretion. The main physiological function of the acid induced antral somatostatin release might be to block the release of gastrin in response to various stimuli.