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Chapter 9 (page 36)
Somatostatin is considered to be a potent vasoconstrictor of the intestinal circulation, and
some of the inhibitory effects in the gastrointestinal tract may be the result of diminished
mesenteric blood flow (Konturek et al. l978). It also suppresses motility of the intestine
and contractions of the gall bladder and it possesses neurotrophic effects. The findings
suggest that somatostatin not only serves as a hypophysiotrophic hormone, but also as a
neurotransmitter (Vale et al. l977).
Somatostatinomas of the pancreas have been documented; patients had
hypoglucagonaemia, hypoinsulinaemia and mild diabetes, with remission of
hyperglycaemia after removal of the tumor (Ganda et al. l977; Larsson et al. l977).
Holle et al. (l985) determined the number of somatostatin-secreting D cells in the
"antrum", pre- and post-operatively, in 20 patients with duodenal and 8 with gastric
ulceration. In patients with a normal population of gastrin-immunoreactive G cells, the D
cells were within the normal range. High G cell values were accompanied by high D cell
values and low G cell values by low D cell values. The G cell to D cell ratio was 8:1 in
duodenal, and 6.6:1 in gastric ulceration. Morphologic coupling of the gastrin-
somatostatin system in the "antrum" was assumed; this was constant in ulcer disease
both before and after vagotomy.
According to Holle et al. (l985) the almost exclusively inhibitory function of
somatostatin, combined with the proximity to glucagon A and insulin B cells in the
pancreas, as well as to parietal and gastrin G cells in the stomach, raises the question of a
paracrine-like mechanism. However, in addition to the direct interaction of somatostatin
D cells with neighbouring cells, adrenergic and cholinergic pathways also appear to exist.
Said and Mutt (l970) isolated a polypeptide with strong vascular effects from porcine
small intestine. Termed vasoactive intestinal peptide (VIP), it was subsequently purified
by Said and Mutt (l972). For some time VIP was considered to be a solely
gastrointestinal hormone; later studies, however, demonstrated VIP in central and
peripheral neurons, suggesting a neurotransmitter function (Larsson et al. l976). It is now
known that VIP nerves have an ubiquitous occurrence in the body, being particularly
numerous in the gastrointestinal, genito-urinary and respiratory tracts (Alumets et al.
l978). In the peripheral autonomic system these nerves were shown to occur in various
regions, including the superior and inferior mesenteric ganglia, and the submucous
(Meissner's) and myenteric (Auerbach's) plexuses of the intestinal wall (Said l978).
Structures believed to exert a sphincteric function receive a particularly rich supply of
VIP nerves, more so than the smooth muscle of adjacent regions. Among these are the
oesophago-gastric junction, the pyloric "sphincter", sphincter of Oddi, internal anal
sphincter, and the openings of the ureters and urethra into the trigonum of the bladder.
The very rich supply of VIP nerves is a consistent finding in the smooth muscle of all
recognized sphincters; it is thought that an evaluation of the density of VIP innervation
may assist in anatomically defining a sphincter (Alumets et al. l978) (Chap. 2).
Using immuno-fluorescent techniques, Polak et al (l974) determined the cellular
distribution of VIP in the mammalian (dog, pig and baboon) gastrointestinal tract,
mucosal samples being taken from the gastric fornix, pyloric "antrum", duodenum,
jejunum, ileum and colon. The distribution of cells was found to be wide; they were
present in all regions examined, the highest number occurring in the colon in all three
species. According to Bloom and Polak (l978) the highest concentration of VIP cells,
more than 31 per mm², occurred in the colon. There were 11 to 30 cells per mm² in the
duodenum, and in the stomach, including the pyloric mucosal zone, the concentration
was 1 to 10 cells per mm². The relative numerical frequency of these cells in the
different gastric mucosal zones was not determined in detail. Small numbers of cells
occurred in the pancreas.
Walsh (l983) pointed out that while VIP was originally thought to be located in
gastrointestinal endocrine-type cells, later data were consistent with a purely neural
localization in the gut; VIP was also distributed throughout the brain and in peripheral
nerves outside the gastrointestinal tract. In the stomach Ferri et al. (l984) found a dense
VIP-containing nerve supply around oxyntic and pyloric mucosal glands. In the
duodenum VIP (and substance P) were present in striking nerve networks in the villi and
muscularis mucosae and around blood vessels. VIP was also immunostained in nerve
bundles and neuronal perikarya between the lobules of Brunner's glands, while very few
fibres reached the proximity of the acinar cells of these glands (Chap. 4).
The biological actions of VIP are numerous and include vasodilatation, lowered blood
pressure, increased cardiac output, glycogenolysis and relaxation of smooth muscle
(Piper et al. l970). VIP release from the gut was demonstrated upon electric stimulation
of the vagus in pigs; significant inhibition of gastric secretion was associated with
enhanced VIP release (Said l978). The physiological role of VIP, however, was
uncertain (Said l978), but it appeared to be implicated in the following actions: it might
serve as a neurotransmitter in the central nervous as well as the peripheral autonomic
systems; its wide distribution in many tissues and the relatively constant plasma values
suggested that it probably acted as a neurotransmitter in a paracrine, rather than in an
endocrine, way (Modlin et al. l978). The VIP neurons have been shown to be under dual
(both vagal and splanchnic) control of the autonomic system; release of VIP into venous
effluent has been correlated with specific physiological mechanisms known to be
mediated via non-cholinergic and non-adrenergic nerve fibres, and elicited by electrical
stimulation of the vagus nerves (Fahrenkrug et al. l977). Vagal stimulation caused a
frequency-dependent increase in the release of VIP; splanchnic stimulation caused a
decrease in the release of VIP, an action which was annulled by alpha-adrenergic
blockade. The inhibitory effect of splanchnic stimulation significantly diminished
vagally induced VIP release.
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