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 following five tyrosine-containing analogs of somatostatin (GIF) were synthesized by the solid-phase method: Tyr-GIF: [Tyr6]-GIF; [Tyr7]-GIF; [Tyr8]-GIF; [Tyr11]-GIF. These analogs except [Tyr8]-GIF were demonstrated to possess almost the same potency to inhibit thyrotropin release stimulated by thyrotropin-releasing hormone as that of synthesized GIF in vivo. [Tyr8]-GIF had potencies less than 0.5% of GIF. They also had the activity to inhibit Nembutal-induced growth hormone rise. The structure-activity relationship and availability of these analogs for radioimmunoassay were discussed.
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PMID:Biological activities of tyrosine-containing somatostatin analogs on inhibition of secretion of thyrotropin and growth hormone. 100 96

The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.
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PMID:Somatostatin and innervation of the heart of the snake Elaphe obsoleta. 197 Apr 54

Sodium pentobarbitone anaesthesia lowered the circulating growth hormone (GH) concentration in immature chickens and reduced basal and stimulated pituitary GH release in vitro. The immunoneutralization of endogenous somatostatin (SRIF), by passive SRIF immunization, overcame the inhibitory effect of anaesthesia on basal GH secretion in vivo, but had no direct effects on GH release in vitro. However, while SRIF immunization restored the resting GH concentration in the anaesthetized birds, it increased greatly the GH level in conscious birds. These results therefore suggest that the inhibition of GH secretion in anaesthetized birds may be partly SRIF-mediated, although a suppression of hypothalamic stimulation may also be involved.
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PMID:Inhibition of growth hormone secretion in anaesthetized fowl: hypothalamic participation. 288 Jul 81

1. The intravenous (i.v.) infusion of somatostatin (SRIF, 1.0 microgram/kg per min) promptly (within 5 min) reduced the growth hormone (GH) concentration in the plasma of conscious adult chickens. 2. The GH concentration progressively declined throughout a 60-min period of SRIF infusion, but was dramatically increased above pre-infusion levels within 5 min of SRIF withdrawal and maintained at an elevated level for at least 30 min afterwards. 3. Sodium pentobarbitone-anaesthesia lowered the basal GH concentration to levels comparable with those in conscious birds infused with SRIF. When administered to anaesthetized birds, exogenous SRIF was unable to further reduce the GH concentration and unable to induce 'rebound' GH release. 4. While thyrotropin releasing hormone (TRH, 10 micrograms/kg) increased the GH concentration in both conscious and anaesthetized birds, only the GH response in the anaesthetized birds was diminished by SRIF infusion. 5. Rebound GH secretion following the termination of SRIF infusion was observed in both conscious and anaesthetized birds injected with TRH. 6. These results demonstrate that SRIF can inhibit basal and TRH-stimulated GH secretion in adult domestic fowl and indicate that anaesthesia disrupts the normal control of GH releases.
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PMID:Somatostatin inhibition of growth hormone secretion in an adult bird: the domestic fowl. 288 73

Plasma and pituitary GH content, in-vitro GH release and somatostatin-like immunoreactivity (SLI) in the stalk-median eminence were studied up to 7 days after making an anterolateral cut (ALC) around the medial-basal hypothalamus. Plasma GH concentration increased within 15 min to a very high level, then fell to a high level which was unchanged for several hours. The GH concentration then steadily decreased between days 2 and 7. The SLI content in the stalk-median eminence decreased to 3.5% of the control value within 3 days. The GH content of the anterior pituitary gland was 58.8% of the control value by 1 week after the operation but the in-vitro sensitivity to somatostatin of the GH cells failed to change. Pentobarbitone injection stimulated GH release in the sham-operated controls but decreased it in the rats with an ALC. These findings suggest that transection of somatostatin-containing fibres is followed by a rapid rise and a lasting high concentration of plasma GH which slowly returns towards lower levels in parallel with a marked depletion of pituitary GH content. In rats with transected somatostatin innervation of the median eminence, sodium pentobarbitone probably decreases GH secretion by depressing the secretion of GH-releasing hormone.
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PMID:Rapid changes in growth hormone regulation and hypothalamic somatostatin after transection of anterolateral pathways to the medial-basal hypothalamus in the rat. 396 96

We have utilized the relative structural simplicity of several short, cyclic, highly active somatostatin analogs in the search for competitive antagonists of somatostatin. During an attempted synthesis of cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr), catalytic hydrogenation of the protected peptide intermediate unexpectedly gave cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] in which the benzyl protecting group on Thr could not be removed even upon prolonged treatment under standard conditions. Injection of this new peptide into the rat completely blocked the inhibitory effects of exogenous somatostatin on GH, insulin, and glucagon release. Indeed, in fasted rats, basal hepatic portal insulin and glucagon levels were significantly increased after analog treatment. Plasma GH levels in Nembutal-anesthetized and stimulated rats were also increased after injection of the analog. These results provide strong evidence that endogenous somatostatin exerts local tonic control of pituitary and pancreatic secretions. The availability of a somatostatin anatagonist should be of considerable value in elucidating the roles of somatostatin in these and many other physiological processes.
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PMID:Somatostatin antagonist analog increases GH, insulin, and glucagon release in the rat. 612 18