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)

The effect of bradykinin (BK) on the release of beta-endorphin-like immunoreactivity (beta-END-LI) in rats was studied in in vivo and in vitro. Intraperitoneal injection of BK at 5 micrograms/100 g body weight resulted in a significant increase in the plasma beta-END-LI level after 15 min. BK at concentrations of 10(-12)-10(-7) M also caused dose-dependent stimulation of beta-END-LI release from the dispersed cells of the anterior pituitary of rats. On gel chromatography, the beta-END-LI released by incubation of the cells with 10(-7) M BK separated into two components; one eluted in the same positions as human beta-lipotropin and the other as human beta-endorphin. BK did not stimulate beta-END-LI release in Ca++-free medium. Addition of 10(-3) M verapamil, 10(-6) M dexamethasone or 10(-7) M somatostatin to the incubation medium inhibited BK-induced beta-END-LI release from the cells. Ouabain (10(-5) M) also stimulated beta-END-LI release, but its effect was not additive with that of BK. These results indicate that BK stimulates beta-END-LI release and that calcium ion is involved in the mechanism of this effect.
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PMID:[In vivo and in vitro effects of bradykinin on the release of beta-endorphin-like immunoreactivity]. 286 30

The effects of 23 agonists on the rates of cellular 32P efflux and lactate dehydrogenase (LDH) release were tested in a perfused rat heart preparation which had been prelabelled in vitro with [32P]Pi. Some 13 compounds produced detectable changes at high doses within 10 min, and in most cases a polyphasic response was observed. Six classes of compound gave rise to substantial effects, as follows. Catecholamines and glucagon produced a transient initial stimulation of Pi efflux, followed by a long-term inhibition of Pi transport and an increased rate of LDH release. These effects were clearly different from the response seen after treatment with dibutyryl cyclic AMP, which had a slower, stimulatory, effect on Pi output in doses which gave rise to a pronounced inotropic effect, and produced a marked increase in both coronary flow and LDH release. Carbachol also gave rise to a large transient stimulation of Pi efflux, which was followed by smaller sustained increase in Pi output without any obvious effect on LDH release. Dibutyryl cyclic GMP had no effect on Pi efflux or LDH release. Insulin decreased the rate of Pi efflux, although the loss rate partially recovered towards the control value after prolonged exposure to the hormone. Insulin had no obvious inotropic effects and produced no change in the rate of LDH release. Corticosteroids increased the rate of Pi efflux, although the loss rate partially declined towards the control value with prolonged exposure to the hormones. Corticosteroids produced a very slight inotropic response, and large doses sometimes increased the rate of LDH release from the tissue. Aldosterone slightly stimulated Pi output. A small, transient and somewhat variable stimulation of Pi efflux was observed with vasopressin and angiotensin, whereas tri-iodothyronine was slightly inhibitory, but adenosine, histamine, spermidine, des-Asp1-angiotensin, prolactin, parathyroid substances, calcitonin and somatostatin had no significant effects under our experimental conditions. Ouabain stimulated Pi efflux in doses that had no detectable inotropic effect. It is suggested that Pi efflux involves the electroneutral transport of NaH2PO4 across the cardiac plasmalemma and that many of the hormonal effects might be explained by changes in the intracellular [Na+] and pH in addition to changes in the intracellular [Pi].
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PMID:Some hormonal effects on myocardial phosphate efflux. 609 15

We have examined the factors regulating the mucosal release of somatostatin-like immuno-reactivity (SRIF-LI) from 1-cm2 sheets of isolated canine gastric antral mucosa mounted in a Ussing chamber. SRIF-LI was released predominantly into the luminal perfusate, was maximal at pH 2.5, 1,987 +/- 319 pg X ml-1 X h-1, and reached a nadir at pH 6.0 of 89 +/- 24 pg X ml-1 X h-1. Increasing extracellular Ca2+ to 10 mM stimulated the release of SRIF-LI at both high and low pH. The Ca2+ ionophore A23187 had no apparent effect at either pH 2.5 or 7.0. LaCl3 stimulated the release of SRIF-LI at pH 7.0 but not at pH 2.5. Ouabain and TMB-8 had no significant effect on the release of SRIF-LI. At pH 7.0, trifluoperazine (TFP) stimulated release of SRIF-LI (80 +/- 10 pg X ml-1 X h-1). EGTA stimulated release of SRIF-LI at pH 2.5 (1,134 +/- 137 pg X ml-1 X h-1) and at pH 7.0 (300 +/- 57 pg X ml-1 X h-1), which was reversed by replacement of Ca2+ (22 +/- 6 pg X ml-1 X h-1). Thus Ca2+ appears to exert a dual effect on the release of SRIF-LI: both an increase and depletion of extracellular Ca2+ release SRIF-LI.
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PMID:A dual role of calcium in release of somatostatin from canine gastric antral mucosa. 614 72

To clarify the effect of islet hormones on pancreatic ductular cell function, we measured the exocrine secretion elicited by 10 pM secretin in the presence or absence of islet hormones using an isolated perfused rat pancreas model. Insulin significantly increased secretin-stimulated pancreatic juice secretion, but not protein secretion. The potentiating effect of insulin on pancreatic juice secretion was concentration-dependent, and the maximal effect was observed with 1 microM insulin. Ouabain, a specific Na+,K(+)-ATPase inhibitor, caused concentration-dependent inhibition of the potentiating effect of insulin without affecting secretin action. Glucagon (100 nM) significantly inhibited secretin-stimulated pancreatic juice secretion and also tended to inhibit protein secretion. A somatostatin analog, SMS 201-995 (10 nM) significantly inhibited both the pancreatic juice and protein secretion stimulated by secretin. The inhibitory effect of SMS 201-995 was concentration-dependent and was maximal at 1-10 nM. These results demonstrate that insulin potentiates the secretory response to secretin, at least partly by increasing Na+,K(+)-ATPase activity, whereas glucagon and somatostatin inhibit this response. Thus, pancreatic islet hormones regulate the secretory function of pancreatic ductular and centroacinar cells.
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PMID:Effect of islet hormones on secretin-stimulated exocrine secretion in isolated perfused rat pancreas. 832 88