Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Our previous studies have shown that stimulation of the anteroventral third ventricle region increases atrial natriuretic peptide (ANP) release, whereas lesions of the anteroventral third ventricle or median eminence block the release of ANP from blood volume expansion, suggesting a critical central nervous system participation in this response. ANP is also produced within neurons that have cell bodies in the rostral hypothalamus and axons that extend to the median eminence and neural lobe. In addition to its natriuretic effect, the peptide can inhibit the release of corticotropin (ACTH) and prolactin, anterior pituitary hormones that are released during stress. To determine the physiologic significance of ANP in the control of basal and stress-induced release of anterior pituitary hormones, highly specific antiserum against the peptide (AB-ANP) was microinjected into the third cerebral ventricle of conscious freely moving male rats to immunoneutralize hypothalamic ANP. In the initial experiment, the antiserum or control normal rabbit serum (NRS) was injected into the third cerebral ventricle to determine the effect of the antiserum on basal release of pituitary hormones. The antiserum had no effect on the concentrations of plasma ACTH, prolactin, or thyroid-stimulating hormone for 3 hr after the injection; however, plasma growth hormone concentration, although unchanged for 2 hr, was markedly elevated at 3 hr. These results indicate that although ANP appears to have no effect on the basal release of the other hormones, it has a physiologically significant inhibitory effect on growth hormone release. The delay of the effect is probably related to the time required for the antiserum to diffuse to the site of action of the peptide, presumably at some distance from the ventricle. Since this effect was demonstrable only after 3 hr, in the stress experiment, the antiserum or NRS was microinjected into the third ventricle 3 hr prior to application of ether stress. The rapid elevation of plasma ACTH in NRS-injected rats was markedly augmented by AB-ANP. Ether also induced a rapid increase in plasma prolactin in the NRS-injected animals, as expected. Contrary to the ACTH response, the maximal increase in plasma prolactin after ether was attenuated in animals preinjected with AB-ANP. In the NRS-injected animals, there was a significant decline in plasma growth hormone after the application of ether that was significantly accentuated by AB-ANP, but this was probably the result of the higher initial levels of plasma growth hormone in the ANP-AB group followed by its disappearance with a half-time similar to that of the NRS-injected group. The decline in plasma thyroid-stimulating hormone after ether stress was unaltered in the animals injected with AB-ANP. The results of these immunoneutralization studies suggest that endogenous ANP does not play a role in thyroid-stimulating hormone release. On the other hand, the endogenous peptide appears to have a physiologically significant inhibitory role in suppressing ACTH release during stress, mediated at least partly by suppression of vasopressin release. Endogenous ANP has a pathophysiologic role in augmenting the prolactin release in stress either by inhibiting release of prolactin-inhibiting factors or, alternatively, by enhancing release of prolactin-releasing factors. Endogenous ANP appears to inhibit resting, without altering stress-induced inhibition of growth hormone release by stimulating somatostatin release and/or inhibiting growth hormone-releasing hormone release or by both actions.
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PMID:The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone. 133 8

To investigate the renal effects of somatostatin in cirrhosis, renal function and plasma and urinary levels of endogenous neurohumoral vasoactive substances were measured in conditions of intravenous water overload (20 mL/kg body wt with 5% glucose) before and during the intravenous infusion of somatostatin (250-500 micrograms/h) in 6 cirrhotic patients without ascites and 17 nonazotemic cirrhotic patients with ascites. Somatostatin induced a significant reduction of renal plasma flow, glomerular filtration rate, and free water clearance in both groups of patients. In patients with ascites, somatostatin also reduced urinary sodium excretion. Changes in renal function were significantly more marked in patients with ascites than in those without ascites and occurred in the absence of changes in mean arterial pressure and plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide. Somatostatin induced a significant reduction in the plasma concentration of glucagon and urinary excretion of prostaglandin E2 that was not related to changes in renal function. These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems.
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PMID:Effects of somatostatin on renal function in cirrhosis. 809 52

Increasing evidence indicates that angiotensin II can be formed by juxtaglomerular cells (JGC) and cosecreted with renin. We investigated the existence of this local renin-angiotensin system in a human JGC tumor, using an in vitro superfusion. The JGC tumor was found concomitantly to release renin and angiotensin I and II. Sequential addition of atrial natriuretic peptide, dopamine, and a somatostatin analog in the superfusion did not affect renin or angiotensin I and II release. The data provide evidence that the human JGC tumor in vitro generates angiotensin II, and supports its possible role as a local in vivo regulator of kidney function.
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PMID:Concomitant release of renin, angiotensin I, and angiotensin II during superfusion of human juxtaglomerular cell tumor. 138 67

The neutral endopeptidase 24.11 (NEP) also called 'enkephalinase' thanks to its inactivation of enkephalins in the brain, was also recently shown to be involved in the degradation of the circulating atrial natriuretic peptide (ANP). Inhibitors of NEP are therefore under clinical trials as new analgesics or antidiarrheal agents, protecting centrally or peripherally released opioid peptides and as novel antidiuretics and anti-hypertensives in prolonging the renal and vascular actions of NEP. It was therefore important from a clinical point of view to investigate the distribution in peripheral tissue of a systemically administered NEP blocker. Different concentrations of the radiolabelled inhibitor [3H]HACBO-Gly have been intravenously injected in rat and the distribution studied using whole-body sections at different times by 'ex vivo' and 'in vitro' autoradiography to investigate differences in tissue accessibility of NEP to a circulating inhibitor. In vivo [3H]HACBO-Gly binding was fully prevented by an excess of unlabelled inhibitor and disappeared rapidly mainly through renal elimination. NEP labelling was prominent in kidney, liver, lung, fat deposits in the neck region, the flat bones of the skull, the mandibula, the vertebrae, the long bones of the limbs, articular cartilages and synoviae. A lower labelling was found in the intestine, the glomeruli and the submaxillary glands. [3H]HACBO-Gly binds also to a limited number of peripheral tissues in which the presence of NEP was yet unknown (bones, parts of adipose tissues. Some tissues, not labelled in vivo, exhibited various degrees of labelling under in vitro conditions (the brain, some portions of the gut, the testes, the prostate). Interestingly, few lobules of the submaxillary glands were much more densely labelled suggesting the possible occurrence of NEP heterogeneity. Except for the brain, the physiological function of NEP in various tissues remains largely unknown, but this ectoenzyme is likely involved in inactivation of regulatory peptides such as: ANP (partially in the kidney), SP in the lung and possibly somatostatin and ANP in bone, ANP in adipose tissue, enkephalin in testes, immune peptidic factors in bone marrow. A part of NEP in bone marrow corresponds probably to the common acute lymphoblastic antigen, CALLA, densely expressed on pre-B cells. Finally, it is important to notice that several tissues containing important concentrations of NEP (brain, testes, prostate, eye, gut, brush border) are inaccessible to the i.v. injected inhibitor thanks to the presence of functional barriers.
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PMID:Neutral endopeptidase 24.11 in rat peripheral tissues: comparative localization by 'ex vivo' and 'in vitro' autoradiography. 188 86

Studies were performed to determine whether the isolated ovine anterior and intermediate pituitary might rhythmically secrete three POMC peptides, ACTH, ir-beta-endorphin (ir-beta-EP), and ir-alpha-melanocyte stimulating hormone (ir-alpha-MSH) in vivo. When blood was taken at 10-min intervals from four ewes with hypothalamo-pituitary-disconnection (HPD), a distinct POMC-peptide and cortisol ultradian rhythm was noted. A comparison of the four HPD ewes with five nonstressed hypothalamopituitary-intact (HPI) ewes revealed that the mean plasma levels of the three POMC-peptides and cortisol were increased, the mean ACTH and ir-alpha-MSH pulse amplitudes were increased, and the mean ir-beta-EP and ir-alpha-MSH interpulse intervals were decreased. When four HPI ewes were subjected to a mild stress, plasma POMC-peptide and cortisol levels increased significantly when compared with the five unstressed HPI animals. In addition, the ACTH and cortisol pulse amplitudes increased and the ir-beta-EP and ir-alpha-MSH interpulse intervals decreased. Although plasma ACTH levels in the stressed HPI and HPD ewes were comparable, mean plasma cortisol levels were 2-fold greater in the stressed HPI animals. To determine whether the ACTH hypersecretion in the HPD ewe might reflect a net reduction in hypothalamic inhibitory influence over ACTH secretion, we examined the effects of dopamine (DA), somatostatin (SS-14), and rat atrial natriuretic peptide [rANF(1-28)] on the secretion of ACTH from cultured ovine anterior pituitary cells. DA and SS-14 did not exert a discernible effect on basal, CRF-, or arginine vasopressin (AVP)-stimulated ACTH secretion. Although basal ACTH secretion was unaffected by rANF(1-28) (10(-12)-10(-8) M), a significant inhibition of CRF- and AVP-stimulated ACTH release was observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of the regulation of the hypothalamic-pituitary-adrenal axis in sheep with hypothalamic-pituitary disconnection. II. Evidence for in vivo ultradian hypersecretion of proopiomelanocortin peptides by the isolated anterior and intermediate pituitary. 197 94

During the past few years more than 30 novel, biologically active peptides have been discovered. Some are produced in endocrine glands and circulate as hormones in the blood; others are contained in the enterochromaffin cells of the gut and may be involved in the regulation of intestinal functions. The vast majority of new peptides, however, have been detected in the central and peripheral nervous systems, where they are synthesized in distinct neurons and stored in neurovesicles. Many of these neuropeptides may be involved in circulatory regulation. There is evidence supporting such a role, especially for centrally located angiotensin, opioid peptides, substance P, neuropeptide Y (NPY), vasopressin, atrial natriuretic peptide (ANP), kinins, corticotropin releasing factor, bombesin, and somatostatin. In this review we discuss the cardiovascular actions of angiotensin, neuropeptide Y, and calcitonin gene related peptide.
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PMID:The role of neuropeptides in cardiovascular regulation. 203 31

Suppression of growth hormone by means of somatostatin has been suggested as a possible adjunct therapy in Type 1 diabetes. To assess the acute effect of the somatostatin analogue SMS 201-995 on kidney function in uncomplicated Type 1 diabetes, 13 normoalbuminuric, normotensive diabetic patients were investigated before and during IV infusion of SMS 201-995 (8 micrograms h-1). A control experiment with infusion of carrier only was also performed. The SMS infusion induced a reduction in the glomerular filtration rate (clearance of 125I-iothalamate) and renal plasma flow (131I-hippuran) from 140 +/- 15 (mean +/- SD) and 550 +/- 69 to 131 +/- 14 (2p less than 0.005) and 492 +/- 73 ml min-1 1.73-m-2 (2p less than 0.001), while filtration fraction and total renal resistance rose (both 2p less than 0.001). Urinary albumin excretion rate, blood pressure, and blood glucose concentration were unchanged. Plasma growth hormone and glucagon were significantly suppressed. The reduction in glomerular filtration rate and renal plasma flow correlated with the fall in glucagon concentration (r = 0.57, 2p = 0.04, and r = 0.63, 2p = 0.02). The urinary flow rate was markedly reduced, urine osmolality increased, and fractional excretion of sodium, calcium, and phosphate were reduced. Arginine vasopressin, atrial natriuretic peptide, angiotensin II, and aldosterone were unchanged by the SMS infusion. Thus SMS 201-995 acutely reduces glomerular filtration rate and renal plasma flow in uncomplicated Type 1 diabetes and has an antidiuretic effect. The effects may be related to suppression of glucagon secretion.
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PMID:Acute effects of a somatostatin analogue on kidney function in type 1 diabetic patients. 214 82

Right heart failure in patients with carcinoid heart disease is a serious prognostic sign. Consideration and adequate timing of valvular operations seem essential for the postoperative outcome. Without any relation to duration or progression of the metastasizing tumor disease, right heart failure developed and increased rapidly for a period of 12 to 17 months in four patients with classic carcinoid syndrome. Invasive hemodynamic and cardiac ultrasound investigations revealed severe carcinoid heart disease, and medical decompensation treatment gradually failed. Tricuspid and pulmonic valve replacement operations resulted in dramatic improvement in three of the patients, and these patients were still free of cardiac symptoms 10, 12, and 38 months postoperatively. One patient died 5 days postoperatively probably of septicemia. The preoperative and postoperative development of the cardiac disease is evaluated clinically, by cardiac ultrasound and plasma atrial natriuretic peptide concentrations, and related to the tumor disease. Surgical anatomy and operative technique are reported, and the beneficial value of prophylactic treatment of the effects of tumor-released vasoactive substances by a somatostatin analog is emphasized.
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PMID:Surgical treatment of carcinoid heart disease. 214 80

If we consider the chemical messengers in the central nervous system, there are about ten classic transmitters--the catecholamines, biogenic amines and amino acids--as opposed to over 50 different neuropeptides. These include previously well-established circulating hormones such as angiotensin, atrial natriuretic peptide, vasopressin and oxytocin, calcitonin and calcitonin gene related peptide (CGRP), the opioid family of peptides, gastrointestinal peptides, pituitary peptides and their releasing factors, and miscellaneous peptides such as the kinins, bombesin, gallanin, and others; all occur as neuropeptides in the brain. There is evidence supporting a role in central cardiovascular control for angiotensin, opioid peptides, substance P, neuropeptide Y, vasopressin, atrial natriuretic peptide, kinins, corticotropin releasing factor, bombesin, somatostatin, and some other peptides. They have been localized in brain areas known to be important for blood pressure regulation, and specific high-affinity peptide receptors have also been discovered. Upon central administration, these peptides produce cardiovascular effects, partly by interacting with other blood pressure-controlling neuroregulators, e.g. catecholamines and GABA. Central inhibition of brain peptide synthesis or interaction with competitive antagonists at the receptor site results in marked cardiovascular effects. Altered peptide levels and activity of synthesizing enzymes, as well as supersensitivity to the pressor action of some brain peptides, have been described in experimental models of hypertension. We are using angiotensin as a model peptide to study the peptidergic control of cardiovascular function.
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PMID:Peptidergic control of cardiovascular function: the angiotensin paradigm. 219 11

Silver tetrafluoroborate (AgBF4) in trifluoroacetic acid (TFA) has been found to cleave the S-trimethyl-acetamidomethyl (Tacm) group or the S-acetamidomethyl (Acm) group without affecting other functional groups in a peptide chain. A newly isolated porcine brain natriuretic peptide-32 (pBNP-32) was synthesized by the combined use of the S-Tacm group and AgBF4 deprotection. The synthetic pBNP-32 was obtained in better yield by the AgBF4 procedure than by the standard I2 procedure. The synthetic pBNP-32 has the highest chick rectum relaxant activity among the known members of the atrial natriuretic peptide-brain natriuretic peptide (ANP-BNP) families. Somatostatin was also synthesized by the Fmoc-based solid-phase method using S-Tacm and AgBF4. In this synthesis, the recently developed reagent tetrafluoroboric acid (HBF4) was applied to cleave the peptide from the resin.
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PMID:Deprotection of the S-trimethylacetamidomethyl (Tacm) group using silver tetrafluoroborate: application to the synthesis of porcine brain natriuretic peptide-32 (pBNP-32). 220 67


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