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)

Specific polyclonal antibodies raised against synthetic thyrotropin-releasing hormone (TRH) infused intracerebroventricularly (ICV) significantly decreased gastric lesions induced by cold restraint stress. The antiulcer effect of immunologic blockade of brain TRH was specific. Normal rabbit serum or antibodies raised against somatostatin, alpha-MSH, Leu-enkephalin, gonadotropin-releasing hormone and atrial natriuretic factor were ineffective. These findings suggest that brain TRH may play an important role in experimental stress ulcer formation.
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PMID:Evidence for a role of brain thyrotropin-releasing hormone (TRH) on stress gastric lesion formation in rats. 211 18

This study evaluated the effect of ACTH and several ACTH fragments on the development of gastric glandular lesions induced by cold-restraint stress in rats. Intracerebroventricular administration of ACTH1-39 dose-dependently (0.1-10 micrograms) inhibited stress gastric lesion formation. Studies with smaller molecular weight forms of ACTH (in a dose equimolar to 10 micrograms of ACTH1-39) revealed that ACTH1-13 and ACTH1-10 were also protective. The ACTH fragments ACTH5-10, ACTH34-39 and ACTH1-17 were without effect. Immunoneutralization of endogenous brain ACTH1-39 significantly increased stress gastric lesion severity. Antisera raised against synthetic somatostatin, gonadotropin-releasing hormone, and L-enkephalin were ineffective. These results with ACTH coupled with our previous demonstration of a protective effect of beta-endorphin suggest that specific brain pro-opiomelanocortin gene products modulate gastric mucosal integrity in response to stress.
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PMID:Brain ACTH prevents stress gastric lesions in rats. 217 16

Nineteen combined renal and segmental pancreatic transplantations with enteric exocrine diversion were performed between May 1984 and September 1985. The one year actuarial patient survival rate and pancreatic graft survival rate were 86 and 66 per cent, respectively. Thirteen pancreatic grafts are presently functioning (two to seven months) and all of the recipients are insulin-free. Although graft cold ischemia time was kept low (a mean of 4.6 hours), a moderate graft pancreatitis developed with a peak serum amylase level of 16.8 +/- 2.2 microkatal per liter. Analysis of the fluid drained through an abdominal drain tube placed at the graft site revealed an amylase activity of 280 +/- 110 microkatal per liter on the first postoperative day and rapidly decreasing to a mean of 15 +/- 5 microkatal per liter on day 6. A pancreatic duct catheter was used to divert the exocrine juice to the exterior during the first few postoperative weeks thereby promoting healing of the pancreaticoenteric anastomosis. The volume of pancreatic juice from the ductal catheter was quite low in the first postoperative days but then rose to reach a plateau level of 500 to 600 milliliters. The amylase activity and the lipase concentration in the pancreatic juice was very high (9,100 +/- 2,450 microkatal per liter and 11.1 +/- 4.4 grams per liter, respectively) during the first postoperative day but then gradually decreased to reach a steady level after four to seven days. Intravenous administration of secretin induced a sixfold increase in the flow of pancreatic juice. An intravenous infusion of somatostatin significantly reduced the flow of pancreatic juice and the amylase activity and lipase concentration in the juice but did not abolish the secretin induced increase in pancreatic secretion.
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PMID:Studies on the exocrine secretion of segmental pancreatic grafts in humans. 243 63

The changes in both the thermoregulatory responses and brain somatostatin (SS) levels produced by ambient temperature (Ta) changes were assessed in rats after they had been equilibrated to each of the Ta for a period of about 90 min. Cold exposure, in addition to elevating hypothalamic SS-levels, led to increased metabolism and cutaneous vasoconstriction at Ta = 8 degrees C. In contrast, heat exposure, in addition to lowering hypothalamic SS-levels, resulted in decreased metabolism and cutaneous vasodilation at Ta = 30 degrees C. Rats were chronically implanted with a hypothalamic cannula to allow intrahypothalamic injection of SS on the conscious rats. Direct administration of SS (0.1-0.3 micrograms) into the preoptic anterior hypothalamic area caused a dose-related rise in colon temperature at three Ta tested. The SS-induced hyperthermia was produced by increased metabolism at Ta = 8 degrees C, whereas at Ta = 30 degrees C, it was caused by cutaneous vasoconstriction. At Ta = 22 degrees C, the hyperthermia was caused by increased metabolism and cutaneous vasoconstriction. Systemic administration of cysteamine, in addition to lowering hypothalamic SS-levels, produced a dose-related fall in colon temperature at Ta of 8 degrees C and 22 degrees C. The hypothermia induced by cysteamine was produced by decreased metabolism at Ta = 8 degrees C, whereas at Ta = 22 degrees C, it was caused by both decreased metabolism and cutaneous vasodilation. The data indicate that the hypothalamic SS-levels mediate normal body temperature responses in rats.
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PMID:Somatostatin: a hypothalamic transmitter for thermoregulation in rats. 256 82

We investigated the effect of somatostatin (SS) in guinea-pig ventricular muscles using a force transducer and a conventional microelectrode method. Instead of a negative inotropic effect in atrial muscles, SS (10(-11) to 10(-7) M) elicited a positive inotropic effect in ventricular muscles in a concentration-dependent fashion, without changing the time course of contraction. The positive inotropic effect of SS was accompanied by a significant enhancement of the slow action potentials and was suppressed by diltiazem and phentolamine. An increase of extracellular Ca2+ concentration or stimulation frequency enhanced the positive inotropic effect of SS. The positive inotropic effect of SS was not suppressed in the presence of propranolol, metoclopramide, cimetidine or indomethacin, and it appeared even under cold conditions. These results suggest that SS has a positive inotropic effect in guinea-pig ventricular muscle, which is at least partly due to an increase in the slow inward Ca2+ current.
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PMID:Positive inotropic effect of somatostatin in guinea-pig ventricular muscles. 257 Aug 76

Previous research has established that growth hormone pulse amplitude declines with increasing age. The purpose of this study was to determine whether this decline is associated with (1) increased pituitary response to somatostatin, and/or (2) increased number or affinity of pituitary somatostatin receptors. In the first study, pituitary slices from young (3-4 months), middle-aged (12-14 months), and old (22-24 months) male Fischer 344 rats were superfused with minimal essential medium (1 ml/min) and fractions collected at 5-min intervals. Tissues were stimulated with 10(-7) M hpGRF (1-44) for 1 min and, 40 min later, with hpGRF in the presence of 5 x 10(-9) M somatostatin-14 or somatostatin-28. Two pituitaries from each age group were superfused simultaneously and the experiment replicated 4 times. Growth hormone release was measured by radioimmunoassay. In a second study, somatostatin receptors in purified pituitary membranes from the three age groups were compared using iodo-[Tyr0]-D-Trp8 somatostatin-14. Animals from each age group were pooled, membranes extracted, and incubated with increasing doses of cold peptide. Binding characteristics were analyzed by Scatchard analysis and Ka and Bmax calculated. Results indicated that (1) basal growth hormone release diminished both with age and somatostatin administration, (2) GRF-induced release of growth hormone was similar in all age groups when data were expressed as percent increase from baseline, and (3) in the presence of somatostatin-14, GRF-induced release of growth hormone was attenuated in old as compared to young or middle-aged rats (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased pituitary response to somatostatin in aging male rats: relationship to somatostatin receptor number and affinity. 257 35

It seems clear from the studies reviewed here that there is adequate evidence to support the concept of a biphasic response of the thyroid gland to cold as first postulated by Moll et al. (1972). The initial response to acute exposure to cold begins at the level of the hypothalamus as a result of either neural stimuli from skin and other areas and/or blood of somewhat lower than normal temperature reaching the hypothalamus (Andersson et al., 1963). As a result, the secretion of norepinephrine and/or dopamine may increase, and serotonin and/or somatostatin may decrease. The net result of these is an increase in the release of TRH from the hypothalamus. This, in turn, stimulates the cascade for the release of TSH from the anterior pituitary gland and thyroid hormone from the thyroid gland. Moll et al. (1972) postulated the lack of a feedback limb in this acute phase, and, indeed, this may be the case. It is possible, however, that certain hormones, such as somatostatin, norepinephrine, T3, and T4 could act in the capacity of feedback inhibitors. Additional experiments will be required to assess this possibility. The transitional link between the acute (less than 1 day) and chronic (greater than 1 day) phases of the response of the thyroid gland to cold could be T4 itself. An increase in the concentration of T4 in plasma has been reported to increase peripheral deiodination of T4 to T3 by kidneys and liver of rats. There are no studies at present to indicate that hepatic conjugation can be increased by elevation of plasma levels of T4 and T3. If it can, these responses would provide adequate reasons as to why peripheral metabolism of thyroid hormones increases during chronic exposure to cold. The time-course for these changes to occur needs to be studied in greater detail to establish the sequence of events following acute exposure to cold. The latter may also increase urinary excretion of T4 and T3 in man, but not the rat. This suggests that another aspect of exposure to cold needing additional study is measurement of the binding affinities of T4 and T3 for their transport proteins during exposure to cold as compared to affinities prior to exposure to cold. If binding affinities are reduced, the amount of free hormones would increase and, consequently the likelihood of being excreted into urine and conjugated by the liver would also increase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Activity of the hypothalamic-pituitary-thyroid axis during exposure to cold. 265 59

The effects of cold exposure on mean arterial pressure (MAP), heart rate (HR) and oxygen consumption (VO2) were examined in conscious, unrestrained rats receiving intracerebroventricular (i.c.v.) injections of bombesin or appropriate control solutions. Cold exposure elicited significant elevations of MAP, HR and VO2 in control-treated rats. I.c.v. administration of bombesin produced dose-related suppressions of cold-induced elevations of HR and VO2, but not MAP. The central nervous system (CNS)-selective somatostatin analog, ODT8-SS, injected i.c.v., reversed the effects of bombesin on HR and VO2 during cold exposure. Intravenous administration of atropine methyl nitrate did not antagonize the effects of bombesin on HR and VO2 during cold exposure. HR and VO2 were strongly correlated in bombesin-treated rats suggesting that this peptide may prevent cold-induced elevations of VO2 through a CNS action on cardiac function.
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PMID:Central nervous system effects of bombesin on the cardiovascular response to cold exposure. 286 99

In the present investigation CNS epinephrine (EPI) biosynthesis was selectively interrupted with specific norepinephrine N-methyltransferase (NMT) inhibitors, SK&F 64139 (Smith, Kline & French Laboratories) and LY 78335 (Eli Lilly & Co. Research Laboratories), to determine the effects of central EPI depletion on basal and cold, thyrotropin-releasing hormone, and hypothalamic somatostatin antiserum induced thyrotropin (TSH) secretion in chronically cannulated rats. Because these NMT inhibitors also are alpha 2-adrenergic receptor blockers, the effects of alpha 2- and alpha 1-adrenergic blockade and alpha 2-activation on plasma TSH were assessed with rauwolscine and corynanthine and B-HT 933, respectively. Serum T4 and plasma corticosterone were also measured. Blockade of CNS EPI synthesis resulted in inhibition of basal and cold and thyrotropin-releasing hormone induced TSH release, suppression of serum T4, and increased corticosterone release. The stimulatory effect of SRIF antiserum on plasma TSH was not altered by SK&F 64139. alpha 2-adrenergic blockade suppressed plasma TSH levels, but not to the same degree as the NMT inhibitors; activation of alpha 2-receptors enhanced TSH secretion. Thus, it is possible that part of the effect of the NMT inhibitors on TSH was due to alpha 2-blockade. alpha 1-adrenergic blockade also lowered plasma TSH. These results indicate that central EPI systems have a stimulatory role in TSH regulation, possibly mediated by alpha 2-adrenergic receptors, cold-induced TSH release is mediated, in part, by EPI, and central EPI systems exert an inhibitory effect on the hypothalamic-pituitary-adrenal axis.
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PMID:Regulation of thyrotropin secretion by the central epinephrine system. Studies in the chronically cannulated rat. 300 95

Pain is a complex phenomenon involving both neurophysiological and psychological components. Pathophysiological mechanisms involve neural pathways, and a variety of pain-producing substances and modulating mechanisms. These include acetylcholine, serotonin, histamine, bradykinin, prostaglandins, substance P, somatostatin, cholecystokinin, vasoactive intestinal polypeptide, noradrenaline and endogenous opioid peptides. In assessing patients with pain, it is essential to evaluate the cause of the pain, its severity, type, location, duration, quality, and response to therapies, among other factors. The measurement of pain is dependent on subjective responses, which are evaluated by methods which have been well developed over the last three decades. Alleviation of pain by non-drug treatments must be considered as well as use of pharmacological treatments. These include psychological support, placebos, relaxation training, biofeedback, hypnosis, heat, cold, physical supports and surgery. Oral drugs are generally preferable to parenteral drugs, as are drugs with few side effects and low addictive liability. Both overtreatment and undertreatment are to be avoided. Patients can be expected to differ in their needs and responses, and economic considerations ought not be ignored. Newer approaches to pain management include self-administration of parenteral drugs, the search for new types of analgesics and appreciation of the relationship between age, sex, race, etc. and the response to analgesics. Tricyclic antidepressants, phenothiazines and the new non-steroidal anti-inflammatory drugs have pointed the way to possible improvements in our ability to tailor specific drugs to the needs of individual patients.
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PMID:The management of pain. 355 78


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