Vagal Control of the Release of Somatostatin, Vasoactive Intestinal Polypeptide, Gastrin-Releasing Peptide, and HC1 from Porcine Non-Antral Stomach

Abstract

We studied the secretion of somatostatin and HCl and the release of vasoactive intestinal polypeptide (VIP) and gastrin-releasing peptide (GRP) from isolated, vascularly perfused, porcine non-antral stomach. Electric vagus stimulation increased acid secretion and the release of VIP and GRP and inhibited somatostatin secretion as determined in the venous effluent. Atropine abolished the HCl response and reversed the somatostatin inhibition to a three-fold increase, whereas GRP and VIP responses were unchanged. Both intra-arterial carbachol (10(-6) M) and GRP (10(-8) M) increased acid secretion and inhibited somatostatin secretion. VIP (10(-8) M) increased somatostatin secretion and had no effect on acid secretion. By immunohistochemistry, somatostatin was localized to both open-type and closed-type cells equally spread in the various parts of the gastric glands without particular relation to the parietal cells. Numerous GRP- and VIP-immunoreactive nerve fibers were seen between the glands. It is concluded that the fundic and antral secretion of somatostatin, investigated in a previous study, are differently regulated. The relation of fundic somatostatin release to acid secretion seems to be complex.

Mucosa of the guinea pig gastric corpus is innervated by myenteric neurones with specific neurochemical coding and projection preferences

“…Results of some studies have strongly indicated involvement of intrinsic neurones (Schubert, 1991;Holst et al, 1992;Schubert et al, 1992;Welsh et al, 1994).…”

Tachykinins stimulate acid and pepsinogen secretion in the isolated porcine stomach

“…Tachykinins could thus, together with cholinergic and possibly gastrin‐releasing peptide neurones, be involved in the vagally mediated increase in acid secretion (Skak‐Nielsen et al . 1988, Holst et al . 1992, Lloyd & Debas 1994).…”

“…We found that both SP and NKA are released by electrical stimulation of the vagus nerves and that they stimulated acid secretion. Tachykinins could thus, together with cholinergic and possibly gastrin-releasing peptide neurones, be involved in the vagally mediated increase in acid secretion (Skak-Nielsen et al 1988, Holst et al 1992, Lloyd & Debas 1994. Other results obtained in rats suggest that tachykininergic neurones in the spinal cord have inhibitory effects on vagally induced acid secretion (Okuma & Osumi 1991).…”

“…This model has previously been shown to be suitable for studies of the effects of neurotransmitters, vagal stimulation and hormones on acid and pepsinogen secretion (Skak‐Nielsen et al . 1988, Holst et al . 1992).…”

“…The stomachs were antrectomized to eliminate the secretion of the tachykinins from that origin (Schmidt et al 1996) and to avoid in¯uence of short intramural re¯exes. This model has previously been shown to be suitable for studies of the effects of neurotransmitters, vagal stimulation and hormones on acid and pepsinogen secretion (Skak-Nielsen et al 1988, Holst et al 1992.…”