It appears that, in smooth muscle, there are two distinct types of Ca2+ channel, a voltage-dependent Ca2+ channel and a receptor-linked Ca2+ channel. The former is activated by decreases in membrane potential and the latter is regulated by drug-receptor interactions. These Ca2+ channels exist as separate channels in the aorta of the adult rabbit and of some rat strains; organic Ca2+ antagonists and sodium nitroprusside selectively inhibit each of these two respective channels. By examining the effects of these two specific antagonists, characterization of the Ca2+ channels in other types of smooth muscle was attempted. In a wide variety of vascular smooth muscle (except aorta of above-mentioned animals), however, these two Ca2+ channels showed some sensitivity to both types of inhibitor. It is proposed that in most types of vascular smooth muscle as well as in gastric fundus and corpus, the two types of Ca2+ channel are functionally not completely separated. These subtypes of Ca2+ channels are at least partly sensitive to both organic Ca2+ antagonists and sodium nitroprusside. Intestinal, genital, and tracheal smooth muscles also seem to have two types of Ca2+ channel. These subtypes of Ca2+ channels are, however, sensitive only to organic Ca2+ antagonists and are not affected by sodium nitroprusside.

Anticholinergics have been used for many years to reduce gastric acid secretion (e.g., in peptic ulcer patients). Because of their side effects and the advent of histamine-2 receptor antagonists, however, anticholinergics are now used much less frequently as antisecretory agents. Recently, a selective antimuscarinic type of anticholinergic, pirenzepine, has been developed. This agent reduces acid secretion and heals ulcers without producing serious side effects, probably by preferentially blocking a certain subtype of muscarinic receptor for acetylcholine (M1 receptor). This article will review the current types and subtypes of cholinergic receptors and the mechanisms by which antimuscarinic agents, including pirenzepine, reduce gastric acid secretion.

A number of peptide hormones and hormone candidates were studied by immunocytochemistry with respect to their appearance and distribution in the developing porcine gastroenteropancreatic region. The hormones of the pancreatic islets were the first to appear. At 4 weeks' gestation (the earliest stage studied), glucagon, insulin, and somatostatin cells occurred in the dorsal pancreatic primordium, whereas pancreatic polypeptide cells occurred in the ventral primordium. At this stage, the pancreatic primordia were made up of strands of endocrine cells, and no ducts or acini were seen. Subsequently, the endocrine cells were separated by the growing exocrine parenchyma; at still later stages, they aggregated in small nests. Not until birth did they form mantle islets with insulin cells in the central core and the other endocrine cell types on the outside. Gastrin cells appeared in the stomach at the 4-wk stage; somatostatin cells appeared about 1 wk later. In the intestines, these two cell types appeared at the 6-wk stage. Cells displaying glucagon immunoreactivity were the first endocrine cells to appear in the intestine. They occurred in the upper small intestine at the 4-wk stage; they later disappeared from this location but appeared instead in the lower small intestine and colon where they remained. Secretin, cholecystokinin, motilin, gastric inhibitory peptide, and neurotensin cells all appeared at the 6-8-wk stage, and were restricted to the small intestine throughout development. Enkephalin immunoreactive cells appeared late during ontogeny (at the 13-15-wk stage) in both the gut and pancreas. Still later (15-17-wk stage), dense accumulations of endocrine cells (Segi's cap) were occasionally observed on the top of villi in the upper small intestine; these accumulations consisted mainly of somatostatin, cholecystokinin, and gastric inhibitory peptide cells. In view of the early appearance of many gastroenteropancreatic endocrine cell types in fetal life, a functional significance of gastroenteropancreatic hormones in the early development of gut and pancreas is likely.

A 16-yr-old man with Burkitt's lymphoma presented with 1 mo of epigastric pain and was found at endoscopy to have gastric ulcers with nodular borders and a duodenal mass lesion. Laparotomy revealed a large pelvic mass and tumor involvement of the stomach, small bowel, and retroperitoneal lymph nodes. Presentation with gastroduodenal disease is unusual, and the endoscopic features of Burkitt's lymphoma have not been previously reported. Gastrointestinal involvement with Burkitt's lymphoma is reviewed, and characteristics of the North American and African varieties are contrasted.

Glucagonlike substances in extracts of intestinal mucosa were already described in 1948 by Sutherland and deDuve (1), who used a bioassay technique for the identification. After the development of the first glucagon radioimmunoassays, Unger and co-workers (2,3) confirmed that intestinal extracts contained peptides that "crossreacted" in the glucagon radioimmunoassay [hence gut "glucagonlike immunoreactivity" (GLI)]. In 1968, the same group discovered that the gut GLIs consisted of at least two peptides, GLI I and II (4), both of which differed immunochemically from pancreatic glucagon and, therefore, necessarily had different chemical structures (4,5). Developments during the last decade in the field of peptide chemistry, particularly improved purification and sequencing techniques, have greatly advanced our knowledge of gut peptides, including the enteroglucagons, and the chemical structure of several of the members of this heterogenous group of peptides is now known. Furthermore, progress in the field of nucleotide and gene technology has also spread to this area of research, and although many problems remain unresolved, the progress made has sufficiently important implications to justify a review of the most recent advances.

Skeletal and cardiac muscle involvement is a recognized feature of the muscular dystrophies. Visceral smooth muscle involvement of the gastrointestinal tract is not as well appreciated. Gastrointestinal symptoms may herald the onset of a muscular disorder and may be the predominant feature of the disorder. In some instances, smooth muscle dysfunction may be the only clinical manifestation of the disease. The gastrointestinal manifestations of the various muscular dystrophies are reviewed. Clinical, radiographic, and histologic features are discussed. Further study of the histopathology and pathophysiology of visceral smooth muscle involvement in the muscular dystrophies will have a substantial impact on treatment that, to a large extent, remains empiric.