Paracrines are synthesized in and released from endocrine cells in the same fashion as hormones. However, the amounts released do not reach the general circulation in concentrations sufficient to produce effects. Instead, paracrines act on cells in their immediate vicinity, reaching them by simple diffusion or perhaps movement through capillaries before being diluted in the general circulation. One can assess the biologic significance of a hormone by correlating its plasma levels with its effects. Similar studies are not possible with paracrines or neurocrines. Current studies make use of specific pharmacologic blocking agents or antisera directed toward these substances. Some investigators have perfused organs in vitro and successfully measured changes in the release of paracrine agents in the small volumes of venous effluent.

At this time, somatostatin is the only GI peptide we know of that functions physiologically as a paracrine (Table 3). It was first isolated from the hypothalamus as growth hormone release inhibitory factor (GHRIF), and it appears to inhibit the release of all peptide hormones. It is now known to exist throughout the GI mucosa and to inhibit the release of all gut hormones. Somatostatin is released by luminal acid and mediates the inhibition of the release of gastrin when the gastric contents are acidified. It also directly inhibits acid secretion from the parietal cells. Vagal activation prevents somatostatin release. It may also act physiologically as a paracrine in the pancreatic islets to regulate insulin and glucagon release.

The only other known significant paracrine agent in gut physiology is histamine. Histamine is not a peptide, but is found throughout the mucosa in endocrine-like cells called ECL cells (enterochromaffin-like). Gastrin stimulates the release of histamine and its synthesis by activating the enzyme histidine decarboxylase present in the ECL cells. Gastrin also stimulates the growth of these cells. Released histamine then stimulates the parietal cells to secrete acid. Histamine also potentiates the effects of gastrin and acetylcholine on acid secretion. This is why drugs like Tagamet (cimetidine) and Zantac (ranitidine) that block histamine H2-receptors are such potent inhibitors of acid secretion.

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