Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

49 cases of myocardial infarction during pregnancy are reviewed from the literature, considering the frequency, pathogenesis, clinical findings, prognosis, treatment, obstetrical conduct including whether abortion is indicated, and finally 17 cases of pregnancy in women with previous heart attacks are summarized. A myocardial infarction is rare, about .01-.075%, more frequent in late pregnancy or the postpartum, and in older women. This series averaged 32.9 years. 88% were due to atherosclerosis. Other risk factors were usually not reported systematically. 56% of the incidents were the 1st heart attack; 44% were preceded by angina; 68% were anterior. Pregnancy affects the EKG and white blood count, but serum enzymes are the same as in nonpregnant women. 29% of these women died, 23 went to term, and 7 gave birth prematurely. 13 labors were spontaneous, 7 required forceps, and 10 were Caesarean births. Fetal loss was 27%. Treatment is the same as that in any heart attack patient, except for lignocaine and use of anticoagulants. Abortion is only necessary in cardiac insufficiency. Delivery should probably involve forceps, epidural anesthesia, and anticoagulatns immediately after delivery, but oxytocin should be avoided. The 17 cases of pregnancy after a heart attack resulted in 1 abortion, 15 term deliveries, 3 new infarctions, and 1 death due to antoher heart attack at term.
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PMID:[Myocardial infarct and pregnancy]. 103 53

The effect of terbutaline sulfate on left ventricular size and performance was studied by M-mode echocardiography in pregnant women with premature labor. Patients with uterine activity initiated during either oxytocin challenge testing or induction of labor served as a comparison group. During terbutaline therapy, heart rate, ejection fraction, and cardiac output increased significantly. End-diastolic volume and systolic blood pressure (BP) were unchanged, and diastolic BP and end-systolic volume fell. No changes in echocardiographic or hemodynamic parameters were present during oxytocin-induced uterine activity. Terbutaline, as currently used to prevent premature labor, is a potent inotropic and chronotropic agent. Pulmonary edema accompanying terbutaline treatment is probably not due to cardiac failure.
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PMID:Terbutaline and maternal cardiac function. 731 Sep 63

The aim of the present investigation was to study the structure of reactively modified rat myocardium (experimental heart failure model) during in vitro organotypical culture, including the direct effect of some hypothalamic nonapeptides (oxytocin) and monoamines (dopamine, noradrenalin). Light and electron microscopic methods were used. The major regularities of structural and functional reorganization of myocardium were determined. Multidirectional nature of ultrastructural changes of cardiomyocytes and of cardiac non-muscular cells was found to depend on direct effect of hypothalamic nonapeptides and monoamines upon myocardium. Adaptogenic role of oxytocin in provision of cardiac muscle protection and vitality is discussed.
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PMID:[Ultrastructural characteristic of reactively modified myocardium cultured in vitro]. 1487 Apr 66

It is now well accepted that the sympathetic nervous system responds to specific afferent stimuli in a unique non-uniform fashion. The means by which the brain transforms the signals from a single type of receptor into an appropriate differential sympathetic output is discussed in this brief review. The detection of and response to venous filling are used for illustration. An expansion of blood volume has been shown in a number of species to increase heart rate reflexly via sympathetic nerves and this effect is primarily an action of volume receptors at the venous-atrial junctions of the heart. Stimulation of these volume receptors also leads to an inhibition of renal sympathetic nerve activity. Thus the reflex response to an increase in plasma volume consists of a distinctive unique pattern of sympathetic activity to maintain fluid balance. This reflex is dependent on neurones in the paraventricular nucleus (PVN). Neurones in the PVN show early gene activation on stimulation of atrial receptors, and a similar differential pattern of cardiac sympathetic excitation and renal inhibition can be evoked by activating PVN neurones. Cardiac atrial afferents selectively cause a PVN GABA neurone-induced inhibition within the PVN of PVN spinally projecting vasopressin-containing neurones that project to renal sympathetic neurones. A lesion of these spinally projecting neurones abolishes the reflex. With regard to the cardiac sympathetics, there is a population of PVN spinally projecting neurones that selectively increase heart rate by the release of oxytocin, a peptide pathway that has no action on renal sympathetic outflow. In heart failure the atrial reflex becomes blunted, and evidence is emerging that there is a downregulation of nitric oxide synthesis and reduced GABA activity in the PVN. How this might give rise to increased sympathetic activity associated with heart failure is briefly discussed.
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PMID:A role for the paraventricular nucleus of the hypothalamus in the autonomic control of heart and kidney. 1560 10

Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, oxytocin administration, hypothyroidism, glucocorticoid, and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the nonosmotic stimulation of arginine vasopressin release with up-regulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. These perturbations are reversed by V2 vasopressin receptor antagonists. In contrast, urinary concentration defects leading to polyuria are vasopressin resistant. They may involve several factors, such as impaired countercurrent concentration secondary to down-regulation of Na-K-2Cl cotransporter. Vasopressin-resistant down-regulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.
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PMID:Vasopressin and aquaporin 2 in clinical disorders of water homeostasis. 1851 89

Among the cardiovascular pathologies, ischemic heart disease is a serious medical problem that can result in cardiac injury and (or) heart failure. The aim of the present study was to test the hypothesis that neuropeptide oxytocin induces cardioprotective effects on ischemia-reperfusion-induced myocardial damage. The functional parameters of isolated Langendorff-perfused rat hearts were recorded before and after global 25 min ischemia and subsequent reperfusion. The infarct size was determined by a computerized planimetric method. The results showed that oxytocin produced negative chronotropic effect even at low concentrations (90-125 nmol/L). Perfusion with oxytocin before ischemia resulted in significant reduction of the infarct size (p<0.01), which was about 66% smaller than that in the control group. To evaluate the functional mechanisms involved, further experiments were performed under conditions of constant heart rate. The lower dose of oxytocin (90 nmol/L), which was ineffective in spontaneously beating hearts, induced a significant decrease of contractility. Elimination of the negative chronotropic effect of oxytocin prevented its cardioprotective action. In conclusion, our results demonstrated an attenuation of the infarct size in oxytocin-treated hearts, indicating a cardioprotective effect of oxytocin. The data suggest that the negative chronotropic action of oxytocin participates in its protective effects on ischemia-reperfusion-induced myocardial injury.
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PMID:Oxytocin exerts protective effects on in vitro myocardial injury induced by ischemia and reperfusion. 1923 77

Neurogenic stress causes sudden acceleration of heart rate and elevation of arterial blood pressure. that may markedly increase the work load of the heart. Several recent clinical studies document significant role of stress in evoking sudden cardiovascular complications. It has been also shown that the cardiovascular responses to stress are significantly exaggerated during the post-infarct cardiac failure. This review emphasises important neuromodulatory role of some neuropeptides in regulation of the cardiovascular system during stress. A number of experimental data provide evidence that intensity of the cardiovascular responses to stress is regulated by neuropeptides. Vasopressin, angiotensin II and interleukin-1beta (IL-1beta) appear to be responsible for exaggeration of the cardiovascular responses to stress whereas oxytocin seems to act in the opposite way. Recent studies performed in our Department provide evidence for differential involvement of angiotensin II AT(1), vasopressin V(1a), IL-1 and oxytocin receptors in regulation of the cardiovascular responses to the alarming stress. Current evidence suggests that the enhanced stimulation of central AT(1) and V(1) receptors as well as the attenuated stimulation of oxytocin receptors account for exaggeration of the cardiovascular responses to the sudden alarming stress during the post-infarct state. Growing number of data indicate that angiotensin II significantly interacts with vasopressin, interleukin-1 and TNF-alpha systems in the central cardiovascular control under resting conditions. Some of the neuropeptides interact also during stress.
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PMID:Role of neuropeptides in central control of cardiovascular responses to stress. 1925 65

The hypothalamic nonapeptide vasopressin is a known player in the pathogenesis of chronic heart failure. According to the large body of clinical evidence, vasopressin has an impact on salt and water imbalance, hyponatremia, and subsequent renal insufficiency - the most common and destructive co-morbidity of patients afflicted with chronic heart failure. Despite the well-documented elevated levels of vasopressin in the blood of such patients, its expression in the magnocellular hypothalamic nuclei and transport to the posterior pituitary has not yet been investigated. In addition, the literature almost lacks the information on the contribution of another member of nonapeptide family, oxytocin, in the pathogenesis of this disease. Here we present a postmortem analysis of vasopressin and oxytocin-immunoreactive neurons and their terminals in the posterior pituitary of 8 male patients (53.8+/-9.3 years) who had died from CHF and 9 male controls (54.6+/-11.8 years). In line with previous clinical reports, our study on hypothalami of chronic heart failure patients revealed a significant increase in the relative profile density (+29%) of vasopressin-positive neurons in the hypothalamic supraoptic nucleus. Consistently we found a significant increase in the relative optic density of vasopressin-immunoreactivity in the posterior pituitary (+33%) of these patients. In contrast, the similar analysis applied for oxytocin neurons revealed no statistically significant differences to controls. In conclusion, our study provides the morphological evidence for activation of vasopressin (but not oxytocin) expression and vasopressin transport to the posterior pituitary in patients with chronic heart failure.
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PMID:Comparison of vasopressin and oxytocin expressions in the hypothalamo-neurohypophysial system of patients with chronic heart failure. 1967 16

Vasopressin (VP) and oxytocin (OT) are mainly synthesized in the magnocellular neurons of the paraventricular (PVN) and supraoptic nucleus (SON) of the hypothalamus. Axons from the magnocellular part of the PVN and SON project to neurohypophysis where VP and OT are released in blood to act like hormones. Axons from the parvocellular part of PVN project to extra-hypothalamic brain areas (median eminence, limbic system, brainstem and spinal cord) where VP and OT act like neurotransmitters/modulators. VP and OT act in complementary manner in cardiovascular control, both as hormones and neurotransmitters. While VP conserves water and increases circulating blood volume, OT eliminates sodium. Hyperactivity of VP neurons and quiescence of OT neurons in PVN underlie osmotic adjustment to pregnancy. In most vascular beds VP is a potent vasoconstrictor, more potent than OT, except in the umbilical artery at term. The vasoconstriction by VP and OT is mediated via V1aR. In some vascular beds, i.e. the lungs and the brain, VP and OT produce NO dependent vasodilatation. Peripherally, VP has been found to enhance the sensitivity of the baro-receptor while centrally, VP and OT increase sympathetic outflow, suppresse baro-receptor reflex and enhance respiration. Whilst VP is an important mediator of stress that triggers ACTH release, OT exhibits anti-stress properties. Moreover, VP has been found to contribute considerably to progression of hypertension and heart failure while OT has been found to decrease blood pressure and promote cardiac healing.
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PMID:Vasopressin and oxytocin in control of the cardiovascular system. 2399 56

Arginine vasopressin (AVP) is a 9-amino acid peptide that is secreted from the posterior pituitary in response to high plasma osmolality and hypotension. AVP has important roles in circulatory and water homoeostasis, which are mediated by oxytocin receptors and by AVP receptor subtypes: V(1a) (mainly vascular), V(1b) (pituitary), and V(2) (renal). Vaptans are orally and intravenously active nonpeptide vasopressin-receptor antagonists. Recently, subtype-selective nonpeptide vasopressin-receptor agonists have been developed. A selective V(1a)-receptor antagonist, relcovaptan, has shown initial positive results in the treatment of Raynaud's disease, dysmenorrhea, and tocolysis. A selective V(1b)-receptor antagonist, nelivaptan, has beneficial effects in the treatment of psychiatric disorders. Selective V2-receptor antagonists including mozavaptan, lixivaptan, satavaptan, and tolvaptan induce highly hypotonic diuresis without substantially affecting the excretion of electrolytes. A nonselective V(1a)/V(2)-receptor antagonist, conivaptan, is used in the treatment for euvolaemic or hypervolemic hyponatremia. Recent basic and clinical studies have shown that AVP-receptor antagonists, especially V2-receptor antagonists, may have therapeutic potential for heart failure. This review presents current information about AVP and its antagonists.
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PMID:Therapeutic potential of vasopressin-receptor antagonists in heart failure. 2440 75


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