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)

Perivascular nerve stimulation of rat livers perfused in situ with erythrocyte-free Krebs-Henseleit buffer at constant pressure in a non-recirculating system resulted in an increase of glucose and lactate production and in a decrease of portal flow. Infusion of somatostatin in different concentrations (2 x 10(-7), 10(-8), 10(-9) mol.l-1) reduced the nerve-mediated activation of glucose release maximally to 66%. There was only a slight effect on the lactate output, the nerve-mediated reduction of portal flow was unaltered. In controls, somatostatin alone had no effect on the metabolic and hemodynamic parameters. In order to differentiate between a presynaptic and postsynaptic mechanism, the noradrenaline overflow was calculated. The unaltered release of the neurotransmitter in the presence or absence of somatostatin excluded a presynaptic mechanism. To mimic the nerve effects on the carbohydrate metabolism and on the hemodynamics, noradrenaline (2 x 10(-7) mol.l-1) was infused instead of the nerve stimulation over a period of 5 min. Somatostatin did not change the endocrine effects of the catecholamine under these conditions. The nerve-dependent effect of somatostatin suggests that other neurotransmitters (e.g. VIP) or mediators (e.g. prostanoids) may be influenced by somatostatin.
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PMID:Modulation by somatostatin of nerve-mediated activation of glycogenolysis in the perfused rat liver. 256 47

The effect of plasma noradrenaline concentrations within the physiological range (less than 5-6 nM) on the endocrine pancreas was investigated in 9 nondiabetic volunteers. Noradrenaline significantly inhibited plasma insulin levels but did not change plasma glucagon and somatostatin concentrations.
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PMID:Effects of physiological increases in plasma noradrenaline on the human endocrine pancreas. 257 94

Cysteamine (CYS) is known to be a quite specific depletor of somatostatin in the rat brain. In the present study we investigated the effect of CYS (100 mg/kg, 300 mg/kg, subcutaneously) on levels of somatostatin-like immunoreactivity (SLI) in the brain and cerebrospinal fluid, on catecholamines in the cortex, and on spectral cortical electroencephalogram (EEG) of rat. SLI was decreased in both the cortex and the striatum (p less than 0.05) of CYS-treated rats, but no change was seen in SLI of CSF. Cortical levels of dopamine, noradrenaline and homovanillic acid were decreased (p less than 0.05) following administration of either dose of CYS. In EEG, during mobility both the frontal and occipital peak (Fp) and mean (Fm) frequencies were slowed (p less than 0.05). Frontally, the amplitude of the frequency bands 1.5-3Hz and 3-5Hz was increased (p less than 0.05). During immobility the Fp and Fm were also slowed. In frequency bands of 3-5Hz, 5-10Hz and 10-20Hz the amplitude was decreased (p less than 0.05), indicating that, in addition to theta frequency, the low voltage fast activity is also affected by CYS. According to our results, both the cortical intrinsic neurons containing somatostatin and also the ascending catecholaminergic systems are affected after the single administration of CYS concomittantly with, but not necessarily related to, changes in different frequency bands in EEG.
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PMID:Effect of cysteamine on levels of somatostatin-like immunoreactivity and catecholamines and on electroencephalogram in the rat brain. 257 Nov 5

Cysteamine (1.95 or 3.90 mM/kg) administered subcutaneously (sc) markedly decreased the open-field activity of the rats, while the structurally related amino acid cysteine had only minor influence. Cysteamine (1.95 or 3.90 mM/kg) reduced the noradrenaline and increased the dopamine and dihydroxyphenyl acetic acid (DOPAC) levels in the hypothalamus. In striatum the drug decreased both the noradrenaline (1.95 or 3.90 mM/kg) and dopamine (3.90 mM/kg) levels without influencing the DOPAC content. Neither the hypothalamic nor the striatal catecholamines are influenced by administration of equimolar doses of cysteine. Cysteamine (1.95 or 3.90 mM/kg) decreased the somatostatin levels both in the hypothalamus and in the striatum without influencing neuropeptide Y (NPY) and corticotropin releasing hormone (CRH) concentrations. Cysteine administered in equimolar doses did not influence the peptide levels in these brain structures. These data suggest that the cysteamine-induced behavioural changes are related to the decrease of brain noradrenaline and somatostatin concentrations. The structurally related amino acid cysteine does not influence the behaviour or the central monoaminergic and peptidergic concentrations in the hypothalamus and striatum of rats.
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PMID:Influence of cysteamine and cysteine on open-field behaviour, and on brain concentrations of catecholamines, somatostatin, neuropeptide Y, and corticotropin releasing hormone in the rat. 257 45

A review of biochemical findings is presented which support the idea that Alzheimer's disease represents a condition for which tetrahydroaminoacridine (tacrine) may have a beneficial effect. There is evidence that clinical and histopathologic hallmarks of the disease relate to cholinergic and serotonergic dysfunction, with less obvious abnormalities in other neurotransmitters (aspartate, dopamine, gamma-aminobutyrate, glutamate, noradrenaline and somatostatin). Clinically relevant concentrations of tacrine may ameliorate the above presynaptic deficits without producing harmful (neurotoxic) effects of aspartate and glutamate. The disease seems to be associated with an early and clinically relevant degeneration of some neurons with cortical perikarya that release these amino acid transmitters. Studies are now required on the effect of tacrine on postulated harmful peptide-bond hydrolase activity within and around such cells.
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PMID:Tacrine, a drug with therapeutic potential for dementia: post-mortem biochemical evidence. 257 13

1. NPY is a 36 amino acid tyrosine-rich peptide. It is one of the most abundant and widely distributed neuropeptides known today within the central nervous system with particularly high concentrations in the hypothalamus and in several limbic regions. 2. NPY seems to coexist with other on neurotransmitters like somatostatin, galanin, GABA and the catecholamines noradrenaline and adrenaline in discrete brain regions. 3. NPY binding sites are widely distributed in the brain. However they do not always overlap with the distribution of NPY-like immunoreactivity. 4. NPY is suggested to be involved in a large number of neuroendocrine functions, stress responses, circadian rhythms, central autonomic functions, eating and drinking behaviour, and sexual and motor behaviour. 5. Psychotropic drugs and neurotoxins can alter the NPY concentrations in discrete brain regions. 6. It is possible that NPY is related to various neurological and psychiatric illnesses, like Huntington's chorea, Alzheimer's disease, Parkinson's disease, eating disorders, and major depressive illness.
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PMID:Neuropeptide Y (NPY) and the central nervous system: distribution effects and possible relationship to neurological and psychiatric disorders. 266 85

We compared the effects of electrical stimulation of the splanchnic nerves and infusions of neuropeptide Y, noradrenaline or a combination of the two on pancreatic vascular resistance and exocrine and endocrine secretion. For these studies we used isolated perfused pig pancreas with preserved splanchnic nerve supply. The exocrine secretion was stimulated with physiological concentrations of secretin and cholecystokinin octapeptide. Noradrenaline and NPY at 10(-8) M both increased pancreatic perfusion pressure. Their effects were additive and similar in magnitude to that of electrical stimulation of the splanchnic nerves at 4-8 Hz. Nerve stimulation as well as NPY and noradrenaline infusions inhibited exocrine secretion, but an additive effect could not be demonstrated. Neither NPY nor noradrenaline could reproduce the stimulatory effect of nerve stimulation on glucagon secretion, nor the weak inhibitory effect on somatostatin secretion. NPY alone had no effect on insulin secretion and did not influence the inhibitory effect of noradrenaline. It is concluded that NPY is likely to cooperate with noradrenaline in the control of pancreatic blood flow, whereas its role in the control of pancreatic secretion is likely to be of minor importance, if any.
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PMID:On the regulatory functions of neuropeptide Y (NPY) with respect to vascular resistance and exocrine and endocrine secretion in the pig pancreas. 267 36

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 micrograms subcutaneously), in seven patients with chronic autonomic failure. 2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged. 3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase. 4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.
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PMID:Prevention of glucose-induced hypotension by the somatostatin analogue octreotide (SMS 201-995) in chronic autonomic failure: haemodynamic and hormonal changes. 269 Nov 74

The cardiovascular, biochemical and hormonal responses to a standard test meal have been investigated in patients with chronic autonomic failure and normal subjects. In autonomic failure there was a rapid (within 15 min), substantial and prolonged fall in blood pressure after the meal. A marked fall in blood pressure also occurred after a liquid meal of similar composition and caloric content, with no change in blood pressure in age-matched subjects with normal autonomic function. In autonomic failure after the test meal the blood pressure reached its nadir (45% fall) after 60 min, and had not returned to pre-meal levels after 3 h. There were no changes in cutaneous and forearm blood flow. In the normal subjects there were no changes in blood pressure after the meal; forearm blood flow fell and cardiac output increased. In autonomic failure there were no changes in plasma noradrenaline levels, unlike the normal subjects. Plasma adrenaline levels were unchanged in both groups. There was a similar rise in levels of plasma renin activity in both groups. The haematocrit and plasma osmolality did not change in either group. Changes in plasma glucose and plasma insulin levels were similar in both groups. The responses of 3 pancreatic gut peptides, neurotensin, pancreatic polypeptide and enteroglucagon, were greater in autonomic failure. Basal levels and responses of vasoactive intestinal polypeptide, cholecystokinin-8 and somatostatin were similar in both groups. The motilin response was greater in normal subjects. We conclude that in patients with autonomic failure there was a rapid, substantial and prolonged fall in blood pressure after a meal. This reduction in blood pressure was not counteracted by an increase in sympathetic nervous activity and other compensatory changes, as occur normally. It was unlikely that osmotic effects of the meal or gut secretions resulted in a significant loss of intravascular fluid into the gut. The fall in blood pressure probably results from vasodilatation within the splanchnic circulation, to which pancreatic and gastrointestinal hormones with vasodilatory actions may contribute.
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PMID:Cardiovascular, biochemical and hormonal changes during food-induced hypotension in chronic autonomic failure. 269 19

A detailed regional distribution of nerve cells and terminals immunoreactive to polypeptides or monoamines was examined in the 5 subdivisions (rostral, mid-dorsal, mid-ventral, caudo-dorsal and caudo-ventral parts) of the nucleus preopticus medianus (POMe) of the rat. In general, immunoreactive nerve cells and terminals are more numerous in the ventral parts of the middle and caudal POMe. Nerve cells immunoreactive to neurotensin (NT), Met-enkephalin-Arg6-Gly7-Leu8 (mENK8) or cholecystokinin-octapeptide (CCK8) are distributed throughout the POMe, while those immunoreactive to luteinizing hormone-releasing hormone (LHRH) are found in the rostral and middle POMe. Nerve cells immunoreactive to substance P (SP) are seen in the middle and caudal POMe and those immunoreactive to somatostatin (SRIF) are scattered in the middle part of the nucleus. The densities of nerve terminals immunoreactive to neuropeptide tyrosine, mENK8, SP or noradrenaline are high throughout the POMe, while nerve terminals immunoreactive to CCK8, LHRH, NT, SRIF or vasoactive intestinal polypeptide are moderate and those immunoreactive to calcitonin gene-related peptide, serotonin or dopamine are sparse. This varied distributional pattern of immunoreactive nerve cells and terminals suggests regional differences in function within the POMe.
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PMID:An immunohistochemical observation of polypeptides and monoamines in the nucleus preopticus medianus of the rat. 275 94


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