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)

Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.
Am J Cardiol 1988 Jul 11
PMID:Neuroendocrine manifestations of congestive heart failure. 329 96

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.
J Am Coll Cardiol 1988 Mar
PMID:Variable arginine vasopressin levels in neonatal congestive heart failure. 334 66

Studies were carried out to demonstrate the presence of the endothelium derived relaxing factor (EDRF) in coronary arteries in situ and the effect of hydroquinone on this factor. The studies revealed the presence of EDRF in coronary arteries of rabbit hearts remaining in situ. EDRF was inactivated by left atrial injection of hydroquinone. In situ constriction of coronary arteries by vasopressin was markedly increased following exposure to hydroquinone, and the dilatory response to acetylcholine was absent. The experiments confirm the presence of the endothelium derived relaxing factor in coronary arteries in situ and its inactivation by hydroquinone.
J Mol Cell Cardiol 1987 Apr
PMID:The vasodilator effect of coronary vascular endothelium in situ: its inactivation by hydroquinone. 349 79

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1986 Apr
PMID:Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system. 351 28

In the past, hemodynamic factors, in congestive heart failure were considered as being of major importance in the production of the major symptoms and signs of the disease: peripheral (increased oxygen extraction, flow redistribution) or central (Starling's law, myocardial contractility). More recently, excessive hormonal compensation has been felt to be more important such as: The renine-angiotensin-aldosterone axis, Circulating catecholamines, Arginin-vasopressin. These hormones are responsible for water and sodium retention, tachycardia and increase in peripheral resistance. Newer agents such as Captopril are effective in blocking the action of these endocrine factors.
Can J Cardiol
PMID:[Treatment of congestive heart failure: new concepts]. 352 15

The effects of 4 weeks of captopril treatment were studied in 10 patients with chronic congestive heart failure (CHF). Acute administration of 50 mg of captopril resulted in an increase in cardiac index and significant decreases in arterial pressure, peripheral vascular resistance and pulmonary capillary wedge pressure. Before treatment, all patients had elevated vasopressin levels (17 +/- 4 pg/ml) relative to decreased plasma osmolality (274 +/- 15 mOsm/kg H2O), and these values were not initially affected by captopril administration (22 +/- 7 pg/ml). However, the relation between arginine vasopressin and plasma osmolality was restored to normal by long-term therapy with captopril (50 mg 3 times daily) (3.0 +/- 1.3 pg/ml; 283 +/- 166 mOsm/kg H2O), which also resulted in sustained improvement of cardiac function. Long-term captopril therapy increased plasma renin concentration from already elevated levels (11 +/- 4 to 32 +/- 8 ng AI/ml X hour) and decreased plasma norepinephrine from 1,054 +/- 244 to 488 +/- 101 pg/ml. Thus, nonosmolar stimulation of vasopressin secretion in CHF can be restored to normal by chronic converting enzyme blockade. The acute vasodilator effects of converting enzyme blockade are not mediated by a reduction of possible vasoconstrictor effects of vasopressin.
Am J Cardiol 1986 Aug 01
PMID:Vasopressin, renin and norepinephrine levels before and after captopril administration in patients with congestive heart failure due to idiopathic dilated cardiomyopathy. 352 57

Mechanically and chemically sensitive receptors in the ventricle have been described histologically and electrophysiologically. Early experiments documented the hypotension and bradycardia that resulted from the intracoronary administration of one of the veratrum alkaloids (the Bezold-Jarisch reflex). Mechanical distension of the ventricles also results in a reflex decrease in heart rate and a reduction in peripheral resistance. Skeletal muscle and coronary vascular resistance appear to be most prominently affected by stimulation of ventricular receptors. Coronary ischemia has also been shown to evoke reflex effects which are attributable to stimulation of ventricular receptors. The resultant bradycardia can be especially ominous in acute myocardial infarction. Changes in myocardial inotropic state have been shown to alter ventricular receptor discharge in experimental animals. This stimulus may evoke reflex changes in peripheral hemodynamics. A variety of humoral substances can alter ventricular receptor discharge and evoke Bezold-Jarisch like responses. These include bradykinin and prostaglandins. PGI2, when given intracoronary in small doses or intravenously in larger doses will lower blood pressure while inhibiting the baroreflex induced tachycardia. It has also been shown in some experiments that PGI2 and arachidonic acid can evoke overt bradycardia and hypotension via a reflex mechanism. The role of prostaglandins in cardiovascular reflex control may be important in pathophysiologic states such as coronary ischemia and heart failure. Ventricular receptors can interact centrally with the arterial baroreceptors to attenuate the baroreflex control of both heart rate and peripheral resistance. Finally, the stimulation of ventricular receptors can alter a variety of humoral substances which are important regulators of cardiovascular and fluid volume homeostasis. These include vasopressin, renin and catecholamines. Those studies which have been done within the last 10 years or so, especially in unanesthetized animals, have demonstrated that the Bezold-Jarisch reflex is more important to cardiovascular control than previously thought. Future work will be necessary to determine the precise role ventricular receptors play in various pathological situations.
Basic Res Cardiol
PMID:Left ventricular receptors: physiological controllers or pathological curiosities? 354 77

Assessment of the functional severity of coronary stenoses has become increasingly important as the intrinsic limitations of coronary angiography have been documented. Videodensitometric coronary flow reserve has been proposed as a means to assess the physiologic significance of a coronary stenosis in humans. This study compared videodensitometric assessment of coronary flow with microsphere quantitation in the closed chest canine model. In five dogs, flow rates were assessed at baseline, after vasodilation with adenosine, after vasoconstriction with vasopressin and during rapid cardiac pacing. The videodensitometric peak density, time to one-half peak density and washout time (time from peak to one-half peak density) were compared at each flow state with flow assessed by microsphere injection. Reproducibility of videodensitometric measurements from two different coronary injections during the same flow state was best with peak density (r = 0.94). Videodensitometric flow ratios (flow state under study to flow at rest) using peak density demonstrated a fair correlation with flow ratios by microsphere (r = 0.81). There was poor correlation between flow ratios when time to one-half peak or washout time was used. Videodensitometric flow measurements used in vivo to assess a wide range of drug-induced coronary flows may not accurately reflect coronary flow measured by microsphere.
J Am Coll Cardiol 1987 Apr
PMID:Assessment of myocardial perfusion by videodensitometry in the canine model. 355 88

Impairment of platelet function commonly occurs after cardiopulmonary bypass, and may result in substantial bleeding. Because desmopressin acetate (a synthetic analogue of vasopressin) shortens bleeding time in a variety of platelet disorders, a controlled clinical trial of intravenous desmopressin was performed in 39 patients with excessive mediastinal bleeding (greater than 100 ml/h) and a prolonged template bleeding time (greater than 10 minutes) more than 2 hours after termination of cardiopulmonary bypass. Twenty-three desmopressin recipients and 16 control patients (no desmopressin) were similar in surgical procedure, pump time, platelet count, template bleeding time and amount of bleeding before therapy (p = NS). Compared with the control group, the patients receiving desmopressin (20 micrograms; mean 0.3 micrograms/kg) utilized fewer blood products (29 +/- 19 versus 15 +/- 13 units/patient; p less than 0.05), especially platelets (12 +/- 9 versus 4 +/- 7 units/patient; p = 0.004), while achieving a similarly effective reduction in mediastinal bleeding (4.8- and 4.3-fold, p = 0.001 for both). Severe platelet dysfunction was partially corrected within 1 hour after desmopressin infusion, during which interval no blood products were administered: the template bleeding time shortened (from 17 to 12.5 minutes, p less than 0.05), whereas the platelet count remained unchanged (at 96 +/- 35 and 105 +/- 31 X 10(3)/mm3, p = NS). The plasma levels of two factor VIII components increased: procoagulant activity (VIII:C) from 0.97 +/- 0.43 to 1.52 +/- 0.74 units/ml (p less than 0.05) and von Willebrand factor (VIII:vWF) from 1.28 to 1.78 units/ml (p less than 0.05); these increases correlated with the shortening of the bleeding time (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1987 May
PMID:Treatment of severe platelet dysfunction and hemorrhage after cardiopulmonary bypass: reduction in blood product usage with desmopressin. 357 53

The potency of various C-terminal fragments of the neurohypophyseal hormone [Arg8]vasopressin [AVP-(1-9)] was determined using different avoidance behavioral test procedures in rats. Passive avoidance behavior was facilitated by these peptides. The fragments [Cyt6]AVP-(5-8) and [Cyt6]AVP-(5-9) were the most potent peptides tested after postlearning injection (consolidation) and preretention treatment (retrieval), respectively, after s.c. treatment. Comparable results were found when the peptides were injected into the lateral brain ventricle, but after this route of administration the peptides were about 3 to 4 order of magnitude more potent as compared to the s.c. route. Pentylenetetrazol-induced retrograde amnesia was reversed by AVP-(1-9) and various C-terminal fragments. In this respect [Cyt6] AVP-(5-9) and [pGlu4,Cyt6]-AVP-(4-9) appeared to be the most potent peptides. Injection of AVP-(1-9) and various C-terminal fragments after the acquisition of pole-jumping avoidance behavior induced resistance to extinction of the behavior. The fragment [pGlu4,Cyt6]AVP-(4-8) was the most potent peptide for this effect. Passive avoidance behavior was attenuated by s.c. administered oxytocin [OXT-(1-9)] and various C-terminal fragments. [pGlu4,Cyt6]-OXT-(4-9), [pGlu4,Cyt6]OXT-(4-8) and [Cyt6]OXT-(5-8) were the most potent of the peptides tested after postlearning administration, whereas [Cyt6]OXT-(5-9) was the most potent sequence after preretention injection. In all experiments the effects of the peptides were dose-dependent and of a long term nature. The results show that C-terminal fragments of the neurohypophyseal hormones potently modulate various aspects of memory processes, as assessed with different avoidance behaviors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Structure activity relationship studies with C-terminal fragments of vasopressin and oxytocin on avoidance behaviors of rats. 357 87


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