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)

Catecholamines acting through beta 1- and beta 2-adrenoceptors cause positive inotropic and chronotropic effects in the human heart. In recent years, however, evidence has accumulated that in the human heart also other receptor systems can affect heart rate and/or contractility. Positive inotropic effects can be mediated by receptor systems acting through accumulation of intracellular cAMP (Gs-protein coupled receptors such as 5-HT4-like, histamine H2, and vasoactive intestinal peptide) or by receptor systems acting independent of cAMP possibly through the phospholipase C/diacylglycerol/inositol-1,4,5-trisphosphate pathway (such as alpha 1-adrenergic, angiotensin II, and endothelin). In the non-failing human heart, however, activation of all these receptor systems induces only submaximal positive inotropic effects when compared with those caused by beta-adrenoceptor stimulation, indicating that in humans the cardiac beta-adrenoceptor-Gs-protein-adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility. On the other hand, at least three receptor systems acting through inhibition of cAMP formation (Gi-protein coupled receptors) exist in the human heart: muscarinic M2-, adenosine A1-, and somatostatin-receptors. Activation of M2- and A1-receptors causes negative inotropic effects in the non-failing human heart: in atria activation of both receptors causes decreases in basal as well as in isoprenaline-stimulated force of contraction, but in ventricles only isoprenaline-stimulated force of contraction is depressed.
Basic Res Cardiol 1992
PMID:Receptor systems in the non-failing human heart. 135 55

Vascular smooth muscle cell hyperplasia is a major component of atherogenesis in various animal models. Angiopeptin, a cyclic octapeptide analogue of somatostatin, markedly inhibits myointimal proliferation in response to endothelial cell injury in the rat carotid artery, rabbit aorta and iliac arteries and in coronary arteries of transplanted rabbit hearts. Angiopeptin does not affect serum lipid profiles in nonhuman primates. It is unlikely, therefore, that its antiproliferative effect is mediated by alterations in cholesterol metabolism. Angiopeptin and other peptide analogues of somatostatin are potent inhibitors of growth hormone release and insulin-like growth factor-1 production. However, inhibition of smooth muscle cell proliferation in vivo is not a property common to all somatostatin analogues. This suggests that plasma growth hormone and growth hormone-dependent insulin-like growth factor-1 production are not physiologic stimuli for myointimal proliferation in vivo. Angiopeptin inhibits 3H-thymidine incorporation into rat carotid artery explants, suggesting a local effect on autocrine or paracrine mechanisms regulating cell growth. In view of its potent inhibitory effect on smooth muscle cell replication, angiopeptin may have clinical utility in preventing restenosis after percutaneous transluminal coronary angioplasty and in preventing accelerated coronary atherosclerosis after cardiac transplantation.
J Am Coll Cardiol 1991 May
PMID:Peptide inhibition of myointimal proliferation by angiopeptin, a somatostatin analogue. 167 36

The concentrations of central neuropeptides, somatostatin (SS) and substance-P (SP), were determined in the different brain regions of young-aged male rats after a long-term administration of anticonvulsants Qingyangshen (QYS), Diphenylhydantoin (DPH), and Carbamazepine (CBZ). The results were compared with Pentylenetetrazol (PTZ)-induced seizure model and normal saline-treated controls. No effects of QYS on the concentrations of SS and SP were found in the rats of four-week or eight-week group. Both of DPH and PTZ increased the SS levels in the midbrain of rats in four-week group. DPH, CBZ, and PTZ also increased the SP levels in the cerebral cortex, striatum, and brain stem of rats in eight-week group. Our present data indicated that the central neuropeptides SS and SP were involved in the processes of epilepsy and antiepilepsy. Since QYS did not influence the contents of SS and SP after a long-term administration, it suggested that the anticonvulsant mechanism of QYS may be different from those of DPH and CBZ, i.e. it may be not due to its effect on the central neuropeptide pathway.
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PMID:The investigation of antiepileptic action of qingyangshen (QYS)--effect of QYS on the concentrations of neuropeptides in rat brain. 171 32

We studied the actions of sandostatin (0.1-1000 nM), an analogue of somatostatin, on human atrial tissues obtained from hearts of 20 patients undergoing corrective cardiac surgery. In 3 preparations showing fast response action potential in normal [K]0 Tyrode solution, sandostatin induced little effect, even at the highest concentration (1 microM). In 10 preparations showing a slow rate of phase-0 depolarization when atrial fibers were depolarized (maximum diastolic potential near -40 mV) in high [K]0 (27 mM), sandostatin at concentrations as low as 1 nM decreased significantly the velocity of the upstroke, and the amplitude of slow response of the action potential as well as the force of contraction. In 6 experiments on spontaneously active atrial fibers (maximum diastolic potential = -53.8 +/- 2.7 mV), sandostatin increased the spontaneous cycle length in a fashion dependent upon concentration. The decrease in spontaneous rate of firing was associated with an inhibition of the late diastolic slope, a change also induced by somatostatin. A longer period of washout, however, (30 min or longer) was required for complete recovery from the depressant effects. Sandostatin (0.1-100 nM) also depressed triggered activity induced by cardiotonic agents. The present findings indicate that sandostatin induces a prolonged action in human atrial cells. Sandostatin may depress abnormal automatic rhythms through an inhibition of transmembrane influx of calcium.
Int J Cardiol 1991 Jun
PMID:Electropharmacological effects of sandostatin in human atrial fibers. 187 80

Static muscular contraction has been shown to increase cardiovascular and ventilatory function in reflex manner. The sensory arm of this reflex arc is comprised of group III and IV muscle afferents. The discharge properties of these muscle afferents whose activation causes the pressor reflex response to contraction were investigated. Group III afferents were more responsive to mechanical stimuli, such as tendon stretch and probing their receptive fields than were group IV afferents. In contrast, group III afferents were less responsive to ischemic contraction than were group IV afferents. Equal percentages of group III and IV afferents were stimulated by potassium, lactic acid and arachidonic acid, each of which are metabolic products of contraction. Adenosine, phosphate and lactate, however, had no effect on the discharge of the afferents. Intrathecal injection of antagonists or antibodies to substance P and somatostatin attenuated the pressor response to contraction by about half, a finding that suggests a role for these 2 peptides in the spinal transmission of the reflex.
Am J Cardiol 1988 Sep 09
PMID:Pressor reflex response to static muscular contraction: its afferent arm and possible neurotransmitters. 245 28

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.
J Mol Cell Cardiol 1989 Jun
PMID:Positive inotropic effect of somatostatin in guinea-pig ventricular muscles. 257 Aug 76

The recent demonstration that intravenous administration of somatostatin, an ubiquitous peptide-like substance, may interrupt paroxysmal supraventricular tachycardia in man has disclosed new perspectives in the assessment of the mechanisms of neuro-humoral cardiac regulation in normal and pathologic conditions. Prospective studies on normal subjects and diabetics with and without autonomic cardiac neuropathy, helped in giving an outlook on the mechanism by which somatostatin acts on the human heart. This substance exerts in vivo a powerful chronotropic and dromotropic influence on sinoatrial and A-V node cells both in normals and diabetics with and without autonomic cardiac neuropathy. This influence is blocked by preventive administration of atropine or atropine plus metoprolol (intrinsic heart rate). Since somatostatin-like-substances have been found in cholinergic postganglionic neurons of the cardiac vagus of some animals, the demonstrated "vagomimetic" action of somatostatin on human cardiac cells seems to support the hypothesis that also the human heart may contain vagal somatostatinergic neurons with modulatory function on the heart rate and rhythm. Present observations disclose new perspectives in the pathophysiology and therapy of cardiac arrhythmias.
G Ital Cardiol 1985 Feb
PMID:[Somatostatin and the cardiovascular system: experiences and prospective use]. 286 Nov 34

Effects of hypothalamic hormone somatostatin on the action potential and contractile force of 54 human atrial preparations obtained at cardiac surgery were studied with standard microelectrode techniques. In the atrial fibres responding to electrical stimuli with fast response action potentials in 4 mM [K]0 Tyrode solution (maximum rate of phase 0 depolarization greater than 50 V/s), somatostatin (10(-7) to 10(-6) M) reduced slightly the duration of action potential and decreased twitch force dose-dependently. In spontaneously active atrial fibres, somatostatin (10(-7) to 10(-6) M) abolished the action potentials in the preparations with low maximal diastolic potential (MDP, -48 +/- 2.8 mV), but induced only mild suppressive effect in the preparations with high MDP (-70 +/- 2.4 mV). When the fibres were depolarized in 27 mM [K]0 Tyrode solution, somatostatin decreased the maximum rate of depolarization and amplitude of the slow response action potentials induced by electrical stimuli. The delayed afterdepolarizations or triggered action potentials induced by high-frequency electrical drive in the presence of epinephrine were also suppressed by somatostatin. The above findings suggest that somatostatin may suppress the abnormal automaticity and the triggered activity in human atrial fibres through a reduction of cellular calcium.
J Mol Cell Cardiol 1987 Feb
PMID:Somatostatin effects in isolated human atrial fibres. 288 22

Kindling was induced in Sprague-Dawley rats by repeated injection of pentylenetetrazol (PTZ, 30 mg/kg, IP). Somatostatin-like immunoreactivity (SLI) and 125I-Tyr-somatostatin binding were measured in different areas of the brain in saline-injected controls, rats receiving PTZ but not kindled (prekindled rats), and kindled rats. Compared to SLI levels in controls, SLI increased (p < 0.01) in the frontal cortex, striatum (p < 0.05 in kindled rats), and hippocampus of both prekindled and kindled animals. Hypothalamic levels of SLI remained unchanged. Compared with the controls, no change was found in somatostatin receptor binding in the frontal cortex, striatum or hippocampus in prekindled or kindled animals. These results suggest that an increased level of somatostatin may be connected to the development and maintenance of kindling.
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PMID:Somatostatin-like immunoreactivity and somatostatin receptor binding in rat brain in pentylenetetrazol-induced kindling. 290 7

We studied antiarrhythmic action of D-Ala 2, Leu 5, Arg 6-enkephalin (dalargin) in experiments on male rats. Dalargin is reported to prevent heart rhythm disturbance and heart electrical stability decrease in experimental coronary occlusion, postinfarction, cardiosclerosis and emotional stress. Dalargin prevents acute myocardial ischaemia-induced increase of cAMP content in blood serum and cardiac muscle, as an indirect feature of its antiadrenergic activity. D-Ala 2, Leu 5, Arg 6-enkephalin leads to a decrease of cAMP content in myocardium and blood plasma, which presumably indicates a decrease of sympathetic tone. The data strongly suggest that cGMP content increase and somatostatin level decrease in cardiac muscle play a significant role in antiarrhythmic action of dalargin.
Int J Cardiol 1993 Jul 01
PMID:The anti-arrhythmic effect of D-Ala 2, Leu 5, Arg 6-enkephalin and its possible mechanism. 834 85


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