Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both glucagon and prostaglandin F2 alpha have been shown to stimulate a chloride-rich choleresis in dogs. This study was performed to ascertain the interrelationship between glucagon and prostaglandin F2 alpha in stimulating bile flow. The experiments were performed using dogs with chronic biliary and gastric fistulas. Initially, the effects of prostaglandin F2 alpha on serum glucagon levels were evaluated. Glucagon administration increased bile volume and chloride secretion as did prostaglandin F2 alpha. Serum glucagon levels during prostaglandin F2 alpha administration were increased significantly over baseline values. During prostaglandin F2 alpha administration, the increase in serum glucagon concentration correlated well with the increase in hepatic bile flow. Administration of somatostatin, a hormone known to inhibit glucagon release, prevented the choleresis produced by prostaglandin F2 alpha while simultaneously eliminating the hyperglucagonemia. Subsequently, the effects of glucagon on bile prostaglandin F secretion and the effect of prostaglandin synthetase inhibition on glucagon choleresis were evaluated. Bile prostaglandin F secretion increased from control values of 101 +/- 27 pg per min (mean +/- S.D.) during bile salt infusion alone to 1,498 +/- 1,086 pg per min during the administration of 1 microgram kg-1 hr-1 glucagon. The prostaglandin synthetase inhibitor, indomethacin, significantly decreased the choleresis, the increased bile chloride secretion and the increased bile prostaglandin F secretion produced by glucagon. The results of this study indicate that prostaglandin F2 alpha-stimulated bile flow is primarily the result of glucagon release and suggest that prostaglandin F2 alpha may be involved in glucagon secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship between glucagon and prostaglandin F in stimulating canine hepatic bile flow. 345 73

Recent advances in understanding of intestinal fluid and electrolyte absorption have paved the way for the development of antidiarrheal agents specific for various points in the secretory and absorptive process. Examples of potential antidiarrheal agents include clonidine and lidamidine in diabetic diarrhea, somatostatin in hormonally mediated diarrhea, and prostaglandin synthetase inhibitors in inflammatory diarrhea. Physiological principles of electrolyte transport that underlie these new developments include the capability in both the small and large intestine of the epithelium in absorbing and secreting water and electrolytes; the responsibility of the villus epithelium for sodium chloride/water absorption and of the crypt epithelium for chloride/water secretion; the existence of a continuum between absorption and secretion determined by the sum of the absorptive and secretory drives on the enterocyte; the role of neuroendocrine transmitters, hormones, and inflammatory elements released systemically or locally as stimuli regulating these processes; the fact that most of these stimuli activate specific receptors on enterocytes; and the altering effect of these stimulus-receptor interactions on intercellular levels of cyclic nucleotides or calcium, in turn producing net secretion by diminishing absorption and/or stimulating secretion. Also under investigation as antidiarrheal agents are calcium and calmodulin antagonists, enkephalins, lithium, berberine, oral organic acids, and chloride channel blockers.
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PMID:Antidiarrheal therapy. Prospects for new agents. 354 47

Continuously superfused rat anterior pituitary cells were used to study the effects of prostaglandins (PGs) and a thromboxane (TX) on the secretion of TSH. Indomethacin, a blocker of PG synthetase, inhibited the amount of TSH secreted in response to TRH. This reduction in TRH responsiveness was overcome by administration of PGE2 in combination with the TRH. Arachidonic acid, a prostanoid precursor, increased the amount of TSH released by TRH. Superfusion with TXB2 or imadazole, an inhibitor of TX synthetase, did not change TSH secretion. PGs A2, B2, D2, F1 alpha, F2 alpha, and endoperoxide analogs U-44069 and U-46619 had no effect on hormone release. PGE1 and E2 both increased TRH-stimulated TSH, but neither compound affected basal output; PGI2 was found to stimulate TSH release. Somatostatin inhibited TRH-induced TSH, but failed to block the effects of the PGs. These studies demonstrate that PGs, but no TXs, play a role in TSH secretion. PGE1 and PGE2 appear to modulate TRH responsiveness, while PGI2 directly stimulates hormone output.
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PMID:Effects of various prostanoids on thyrotropin secretion by superfused anterior pituitary cells. 678 40