On the interaction between intragastric pH and electrical vagal stimulation in causing gastric acid secretion and intraluminal release of gastrin and somatostatin in anesthetized rats

The effect of electrical vagal stimulation (5 V, 2 ms, 2, 5 and 10 Hz) on gastric acid secretion and on the intragastric release of gastrin and somatostatin was studied in anesthetized rats. The gastric lumen was perfused with Dextrane T 70 (21 g/1) at 3 different rates (2.0, 0.15 and 0.035 ml/min). pH as well as gastrin and somatostatin levels were measured in the perfusate. At a perfusion rate of 2 ml/min electrical vagal stimulation (10 Hz) reduced pH of the perfusate from 3.8 to 2.6. Neither gastrin nor somatostatin levels were influenced. At a perfusion rate of 0.15 ml/min pH fell to 1.87 during vagal stimulation at 10 Hz. During this period the somatostatin levels in the perfusate increased approximately 7‐fold. No effect on gastrin release was observed. When the stomach was perfused with Dextrane at a rate of 0.035 ml/min. pH was lowered to 1.20 during vagal stimulation at 5 Hz. The somatostatin level increased approximately 14‐fold and the gastrin levels 6‐fold. In order to study the effect of low pH per se the stomach was perfused with 0.1 M HCl. Perfusion of the stomach with 0.1 M HCI (pH1.2) at a rate of 0.035 ml/min caused a small (3‐fold) increase in somatostatin levels. In conclusion, electrical vagal stimulation or low antral pH alone had minor effects on somatostatin or gastrin release. However, when intragastric pH was <2, electrical vagal stimulation increased the intraluminal release of somatostatin and to a lesser extent that of gastrin. We suggest that both somatostatin and gastrin cells are activated by vagal stimulation at low antral pH. Less gastrin was found to be released in comparison to somatostatin, which may be due to inhibition of the gastrin cells by the somatostatin simultaneously released.