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)

Recently it has been shown that, after a meal, blood pressure may fall in the elderly, in patients with autonomic failure and in patients on haemodialysis. This review deals with the available data on postprandial blood pressure reduction, the clinical significance and some pathophysiological hypotheses. The mechanism is not fully understood, but postprandial blood pressure reduction seems to be related to glucose related factors, since blood pressure only falls after oral glucose loading, but not after oral fructose, fat or protein loading. Vasoactive gastrointestinal peptides may play a role in the glucose induced vasodilation of splanchnic vasculature, but attempts to identify such peptides have been unsuccessful. The role of insulin in postprandial blood pressure reduction remains to be elucidated, but it does not appear to have any influence on systemic vasodilation or baroreflex response. Although the clinical significance of postprandial blood pressure reduction remains uncertain, patients can be advised in several ways on how to avoid this symptom. Treatment of hypertension, small carbohydrate meals, caffeine and treatment with the somatostatin analogue SMS 201-995 may have a beneficial effect. Patients on haemodialysis with symptomatic hypotension should not consume meals during the procedure.
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PMID:Postprandial blood pressure reduction. 221 39

It has been known for several years that blood pressure in the elderly may fall after a meal. Although the mechanism is not fully understood, postprandial blood pressure reduction seems to be related to glucose related factors, since blood pressure only falls after oral glucose loading, but not after oral fructose, fat or protein loading. Vasoactive gastrointestinal hormones may play a role in the glucose induced vasodilation of splanchnic vasculature, but attempts to identify such hormones were unsuccessful. Therefore we suggest that interference of insulin with a sympathetic response diminished by age or disease to splanchnic vasodilation, may be responsible for the postprandial fall in blood pressure in the elderly. However, vasodilator effects of insulin or a baroreflex response diminished by insulin do not seem to be involved. Although the clinical significance of postprandial blood pressure reduction remains uncertain, several advises can been given. Treatment of hypertension, small carbohydrate meals, use of caffeine before a meal or treatment with the somatostatin analogue SMS 201-995 may have a beneficial effect.
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PMID:[Reduction in blood pressure after meals in the elderly. A review article]. 267 21

The effect of somatostatin (SS, 1 X 10(-7) M-5 X 10(-6) M) was studied on the electrical and mechanical properties of isolated atria of the guinea-pig. On spontaneously beating right atria, SS produced a dose-dependent negative inotropic effect which was accompanied by a decrease in atrial rate and a prolongation of the sinus node recovery time. In electrically driven left atria, SS produced a dose-dependent negative inotropic effect which occurred concomitantly with a decrease in the amplitude and duration of the plateau phase of the action potential of atrial fibres. SS also decreased the amplitude and maximum rate of depolarization of the slow action potential as well as the amplitude of the slow contractions induced by isoprenaline and caffeine in K-depolarized atrial fibres. The negative inotropic effect of SS varied with the concentration of Ca and Na in the bathing media and the frequency of stimulation. SS, 1 X 10(-6) M and 5 X 10(-6) M, decreased 45Ca uptake in electrically driven atria. All these results suggest that the negative inotropic effect produced by SS on rat isolated atria is related to its ability to reduce Ca influx via the slow inward Ca current.
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PMID:Negative inotropic effect of somatostatin in guinea-pig atrial fibres. 286 1

We describe a patient with severe orthostatic hypotension in whom tilt table conditioning had a striking, beneficial effect. Upon presentation, the patient was unable even to sit, and the deconditioning associated with prolonged bed rest worsened his autonomic dysfunction. Although he was sensitive to the pressor effects of vasoconstrictor drugs (dihydroergotamine, caffeine, and a somatostatin analogue), these agents failed to stabilize his walking blood pressure. With drug therapy, however, the patient could maintain an adequate blood pressure while performing isometric exercises on a tilt table, whose angle was gradually increased during three weeks. After this conditioning program, pressor drug therapy made it possible for the patient to walk. Although the physiologic basis for this therapeutic response is unclear, our results indicate that tilt table conditioning may be an important adjunct to drug therapy in patients with severe orthostatic hypotension.
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PMID:Treatment of orthostatic hypotension: interaction of pressor drugs and tilt table conditioning. 317 58

We studied the effects of acute, intraperitoneal administration of caffeine on serum thyrotropin (TSH), growth hormone, prolactin, thyroxine and 3,3',5-triiodothyronine in rats. Caffeine lowered serum TSH and GH in a dose-dependent manner with ED50 values of 30 and approximately 50 mg/kg, respectively. TSH levels were depressed 1 to 6 hr after injection and correlated with serum caffeine levels greater than 20 micrograms/ml. The decrease in serum TSH was followed by decreases in serum 3,3',5-triiodothyroxine and thyroxine 4 hr after caffeine administration. Theophylline and theobromine had effects similar to those of caffeine on hormone levels. Caffeine did not significantly affect hormone secretion when incubated directly with rat pituitaries in vitro. Administration of antisomatostatin antiserum to rats blocked the inhibitory effects of caffeine on serum GH levels, suggesting that caffeine inhibits GH and TSH secretion by releasing hypothalamic somatostatin.
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PMID:Effects of caffeine on anterior pituitary and thyroid function in the rat. 610 18

The effect of somatostatin on the catecholamine (CA) release from the chromaffin cells was determined on the isolated dog adrenals perfused with 1.8 mM Ca2+ containing fluid except indicated. The extremely low concentrations of somatostatin (0.18 nM-18 nM) were found to stimulate acetylcholine (Ach, 5 microM)-evoked CA release with the maximum response (by 114% above control) at 1.8 nM but the relatively high concentrations (61, 610 nM) caused an inhibition. Somatostatin (6.1 nM) also facilitated excess K+ (15 mM)-induced CA release but failed to enhance the release evoked by a Ca2+ ionophore, A23187 (50 microM) and the release by caffeine (50 mM) under the condition of Ca2+-free. Somatostatin by itself did not affect significantly on the basal release of CA. Elevation of Ca2+ concentrations from 1.8 mM to 5 mM in the perfusion fluid reduced the stimulatory and inhibitory effect of somatostatin. It is possible that somatostatin enhances CA release by facilitating the influx of Ca2+ via the potential-sensitive permeability channel when chromaffin cells are depolarized. The present results provide the first demonstration that somatostatin stimulate the release of CA from the adrenal gland suggesting that somatostatin may function as a facilitatory modulator of the response to ACh at chromaffin cells.
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PMID:Facilitation of stimulation-evoked catecholamine release by somatostatin in dog perfused adrenal glands. 612 82

The respiratory stimulants caffeine and theophylline are able to control apneic spells in premature newborns. However both substances have goitrogenic properties in rats on low-iodine diet. They lower T4 serum levels and inhibit TSH- and GH-release probably by enhancing hypothalamic somatostatin secretion. The retrospective study described here was carried out in an attempt to clarify whether treatment of premature children with methylxanthines has adverse effects on thyroid function. The results are as follows: 1) There is no significant correlation between caffeine- and theophylline-concentrations and circulating T4 levels in single blood specimen of unselected premature infants. 2) In none of the infants was a low T4-serum value accompanied by a rise in serum TSH during methylxanthine treatment. Thus methylxanthines are not associated with the induction of primary hypothyroidism but the possibility of tertiary hypothyroidism cannot be excluded. In order to avoid adverse effects on thyroid function the lowest therapeutically active dose should be chosen.
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PMID:T4 levels in methylxanthine-treated premature newborns. 667 76

Male rats were treated i.p. with either 5 mg/kg amphetamine, 3 and 30 mg/kg cocaine or 100 mg/kg caffeine and killed after 30 min. Brains were sectioned and processed for radioactive in situ hybridization histochemistry for the labelling of either c-fos, enkephalin, substance P, neurokinin B, choline acetyltransferase, somatostatin or adenosine A2A receptor messenger RNA. The distribution of c-fos messenger RNA was investigated both at the regional level using film autoradiography, and at the cellular level using emulsion autoradiography. All drug treatments except 3 mg/kg cocaine induced an increased level of c-fos messenger RNA in cells that had a neuron-like morphology. The cells that contained the c-fos messenger RNA were identified by making pairs of 5-microns sections in which one section was processed for c-fos messenger RNA and the other was processed for one of the other messenger RNA species. After amphetamine treatment, only some 10% of the cells in the striatum were labelled, and to a variable extent. Instead there was prominent labelling of a band in the cortex that runs parallel to the cortical surface. There was also a moderate degree of labelling in the nucleus accumbens. c-fos-positive cells were substance P-positive and negative for enkephalin or A2A receptor messenger RNA. Cocaine (30 mg/kg) induced a modest labelling in the caudate-putamen, as well as in the accumbens. With cocaine treatment (30 mg/kg), about 30% of striatal neuron-like cells were c-fos labelled. Most c-fos-positive cells were substance P-positive, but none of the c-fos-positive cells were enkephalin-positive or A2A-receptor-positive. Cocaine (3 mg/kg) had no significant effect on c-fos. Caffeine gave rise to a strong hybridization signal in the caudate-putamen, particularly the dorsolateral part. No other region examined differed significantly from control. With caffeine treatment, about 73% of neuron-like cells were c-fos labelled in the lateral striatum, but labelling was much less pronounced in the medial part or in the accumbens. c-fos-labelled cells were found in enkephalin-positive and enkephalin-negative, substance P-positive and substance P-negative, neurokinin B-positive and neurokinin B-negative groups. No choline acetyltransferase-positive or somatostatin-positive cells were found that were also c-fos-positive with any of the treatments. We conclude that each of the different CNS stimulant drugs induces a highly specific pattern of c-fos messenger RNA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differences in the regional and cellular localization of c-fos messenger RNA induced by amphetamine, cocaine and caffeine in the rat. 752 Jan 34

Calcitonin gene-related peptide (CGRP) is a neurotransmitter present in the peripheral ends of sensory neurons of the gut and may modulate reflexes of the enteric nervous system. We studied the release of CGRP in normal human gallbladders and in those containing gallstones to test the hypothesis that abnormalities of regulation of CGRP release participate in gallstone formation. Human gallbladder strips were obtained from histologically normal organs removed during liver surgery (n = 8) or from patients operated upon for symptomatic cholelithiasis (n = 14). After removal of the mucosa, muscle strips were superfused with oxygenated Kreb's buffer in an organ bath at 37 degrees C. Pharmacologic agents were added to the superfusate and samples were collected at 2-min intervals for analysis. CGRP release was measured by a sensitive and specific radioimmunoassay and adjusted for tissue weight. In normal gallbladders, CGRP release was stimulated sixfold over basal by capsaicin (10(-5) M) to 363 +/- 75 pg per gram of muscle per 2 min. This release was abolished by addition of somatostatin (SS) or the neural blocker tetrodotoxin (TTX). Lesser degrees of CGRP release were observed after nonspecific stimulation with K+ or phosphodiesterase inhibition with caffeine. In gallbladders with gallstones, capsaicin-induced CGRP release was 74 +/- 16 pg per gram of muscle per 2 min (20% of normal, P < 0.001). Release induced by caffeine and K+ was also inhibited compared to normal gallbladder strips. Release of CGRP from diseased strips was abolished by TTX and inhibited by SS to degrees similar to normal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired release of gallbladder calcitonin gene-related peptide in human gallstone disease. 779 41

Single-cell microfluorimetry techniques have been used to examine the effects of acetylcholine (0.1-100 microM) on the intracellular free calcium ion concentration ([Ca2+]i) in a human-derived pancreatic somatostatin-secreting cell line, QGP-1N. When applied to the bath solution, acetylcholine was found to evoke a marked and rapid increase in [Ca2+]i at all concentrations tested. These responses were either sustained, or associated with the generation of complex patterns of [Ca2+]i transients. Overall, the pattern of response was concentration related. In general, 0.1-10 microM acetylcholine initiated a series of repetitive oscillations in cytoplasmic Ca2+, whilst at higher concentrations the responses consisted of a rapid rise in [Ca2+]i followed by a smaller more sustained increase. Without external Ca2+, 100 microM acetylcholine caused only a transient rise in [Ca2+]i, whereas lower concentrations of the agonist were able to initiate, but not maintain, [Ca2+]i oscillations. Acetylcholine-evoked Ca2+ signals were abolished by atropine (1-10 microM), verapamil (100 microM) and caffeine (20 mM). Nifedipine failed to have any significant effect upon agonist-evoked increases in [Ca2+]i, whilst 50 mM KCl, used to depolarise the cell membrane, only elicited a transient increase in [Ca2+]i. Ryanodine (50-500 nM) and caffeine (1-20 mM) did not increase basal Ca2+ levels, but the Ca(2+)-ATPase inhibitors 2,5-di(tert-butyl)-hydroquinone (TBQ) and thapsigargin both elevated [Ca2+]i levels. These data demonstrate for the first time cytosolic Ca2+ signals in single isolated somatostatin-secreting cells of the pancreas. We have demonstrated that acetylcholine will evoke both Ca2+ influx and Ca2+ mobilisation, and we have partially addressed the subcellular mechanism responsible for these events.
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PMID:Intracellular Ca2+ signals in human-derived pancreatic somatostatin-secreting cells (QGP-1N). 781 49


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