Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overall 210 patients aged 60-74 years suffering from coronary heart disease associated with chronic circulatory failure, stages I, IIA and IIB, 53 patients aged 45-59 years and 20 healthy persons aged 45-74 years were examined for the renin-angiotensin-aldosterone system and antidiuretic hormone. Renin activity, the concentration of aldosterone and vasopressin in blood plasma were investigated by radioimmunoassay. In the initial stage of heart failure, the elderly persons showed up more marked renin activation in blood plasma, followed by its lowering as decompensation progressed as well as an increase in the concentration of aldosterone and vasopressin, which resulted in the progress of circulatory failure.
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PMID:[The renin-angiotensin-aldosterone system and antidiuretic hormone in chronic circulatory failure in elderly subjects]. 144 Feb 54

Blood platelets participating in the formation of haemostatic plugs or thrombi are likely to be exposed to combinations of several agonists. We have found that platelet aggregation and the release reaction are enhanced by combinations of the hormones adrenaline, noradrenaline, vasopressin and 5 hydroxytryptamine acting synergistically at levels obtained in circulating blood for three of these hormones. If surges of adrenaline and other hormones sensitize platelets this may provide a link between some of the risk factors and coronary heart disease.
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PMID:Platelet activation by circulating levels of hormones: a possible link in coronary heart disease. 652 43

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

Sudden cardiac death is mainly caused by arrhythmic events, triggered by ischemia. About half of the affected persons had no previous diagnosis of coronary heart disease, thus rendering them practically unreachable for specific preventive measures. This fact makes it necessary to optimize reanimation conditions. The establishment of international reanimation standards (ILCOR) has stimulated an intensified scientific evaluation of therapeutic options. While the use of vasopressin, adrenaline and reanimation by bystanders is being evaluated at the moment, amiodarone has not fulfilled the expectation of reducing mortality. Secondary prevention of sudden cardiac death after cardiac events is based on betablockers, ACE inhibitors and antilipemic therapy. Guidelines on prevention of sudden cardiac death also recommend aldosterone blockade and n-3-fatty acids. Persons at highest risk gain most from the use of ICDs, yet it has not been shown that their use immediately after myocardial infarction reduces mortality.
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PMID:[Sudden cardiac death (SCD) and guidelines for SCD]. 1502 98

The present study was undertaken to investigate alteration in plasma levels of copeptin, a stable fragment derived from provasopressin, in patients with coronary heart disease. We measured plasma level of copeptin in 21 patients with coronary heart disease (CHD) and 12 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student's t-test and one-way analysis of variance were used for statistical analyses. Correlations between variables were tested by simple linear regression analysis. The plasma level of copeptin was significantly increased in patients (43.07 +/- 17.08 vs 11.13 +/- 5.73 pmol/l in controls, P < 0.01) and was further increased, by 60%, to 68.71 +/- 16.81 pmol/l on day 1 after therapy with percutaneous transluminal coronary angioplasty (PTCA) and stent (P < 0.05). On days 3 and 7 after therapy, the levels were greatly decreased, to 38.82 +/- 19.00 and 32.10 +/- 14.00 pmol/l, respectively, from that before therapy (all P < 0.05) but were higher, by 249% and 188%, respectively, than that of controls (all P < 0.01). The results suggest that the vasopressin system is activated in patients with CHD as indicated by changes in copeptin level, especially after PTCA and stent therapy. As a potential risk factor for CHD, plasma copeptin activation might have important clinical significance in terms of early intervention in patients with CHD.
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PMID:Plasma levels of copeptin in patients with coronary heart disease. 1933 89