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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Understanding of the pathophysiology of heart failure has advanced over the last decade, resulting in new therapeutic advances. Convincing data exist that angiotensin-converting enzyme (ACE) inhibition and adrenergic blockade are the most important therapies and have the capacity to improve survival and lower morbidity. Higher doses of both ACE inhibitors and beta-blockers appear to provide additional benefits. The aldosterone antagonist spironolactone, when used in severe heart failure, provides additional survival advantage when added to standard triple therapy. Angiotensin receptor blockers have not been shown to be superior to ACE inhibitors, and their role in heart failure treatment requires further investigation. No trial's data support the use of inotropic agents or calcium channel blockers in heart failure. A number of new therapeutic agents, including vasopressin antagonists and tumor necrosis factor-alpha receptor antibody are in phase II and III clinical trials. If proved beneficial, they may provide new treatment options for patients with heart failure. Nevertheless, the current challenge is to increase the use of proven therapies, namely ACE inhibitors and beta-blockers, to improve outcomes in the rapidly growing population of patients with congestive heart failure.
Curr Opin Cardiol 2000 Jul
PMID:Update on recent clinical trials in congestive heart failure. 1113 94

Aging is accompanied by significant cardiovascular modifications, both structural and functional. A slight degree of left ventricular hypertrophy develops, while the resting heart rate and early filling rate are somewhat decreased. In contrast, end-diastolic and end-systolic dimensions, stroke volume, and ejection fraction are largely unchanged. The effort tachycardic and inotropic responses are clearly attenuated, whereas the concomitant increase in end-diastolic diameter is enhanced. Large arterial conduits become less distensible and somewhat hypertrophic. Total blood volume is reduced, whereas total peripheral resistance is moderately increased. Neurohumoral systems relevant to cardiovascular regulation are nonuniformly affected by aging: the sympathetic nervous system is overactive and the circulating levels of vasopressin and atrial natriuretic factor are enhanced, while the activity of the renin-angiotensin system is blunted. Elderly individuals have altered cardiovascular homeostasis, with a typical propensity to postural and postprandial hypotension. "Spontaneous" blood pressure variability is increased, whereas heart rate variability is diminished. Vagally mediated chronotropic responses, including those dependent on baroreflex modulation, are attenuated, although end-organ (cardiac) parasympathetic responsiveness is exaggerated. Arterial baroreceptor control of blood pressure is largely preserved in advanced age, whereas cardiopulmonary-mediated reflex responses are definitely impaired.
Am J Geriatr Cardiol
PMID:Modifications of the cardiovascular system with aging. 1177 13

Vasopressin is secreted by the neurohypophysis influenced by many variables; among them the most important and known is the osmotic pressure (osmotic regulation) of body fluid. Other factors that modify this hormone's secretion are changes in blood volume and blood pressure, which contribute significantly to hemodynamic recovery. Vasopressin receptors are located in different sites, and their stimulation generate also generates different physiological responses. The receptors are of two types, V1 and V2. The usefulness of exogenous vasopressin has been proven in many clinical situations, refractory cardiac arrest, septic shock, vasodilator shock, postcardiotomy shock, and vasoplegic shock, with promising results. At present, enough scientific support exists for the use of this antidiuretic hormone (vasopressin) in clinical practice.
Arch Cardiol Mex
PMID:[Vasopressin: uses in cardiovascular practice]. 1241 1

Pharmacologic clinical trials in heart failure (HF) have provided substantial advances in effective treatment of this condition, moving us from our focus on short-term symptom relief to an expectation of substantial improvement in long-term clinical outcomes for our patients. Based on an appreciation of the importance of neurohormonal activation in the pathophysiology of HF, clinical trials have demonstrated the value of angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in impeding the progression of HF and in reducing morbidity and mortality for patients with this condition. Clinical trials have further demonstrated the benefits of digoxin in improving symptoms and reducing hospitalization frequency, as well as in aldosterone blockade, at least in patients with severe symptoms. Given the ethical imperative to treat with ACE inhibitors, the angiotensin receptor antagonists have been difficult to study; nevertheless, their value is becoming increasingly clear, particularly for patients intolerant of ACE inhibitors. Trials with several classes of newer agents-cytokine antagonists, endothelin receptor blockers, and vasopeptidase inhibitors-have recently yielded disappointing results. Early results with vasopressin receptor antagonists provide some promise of long-term benefit. Clinical trials have provided significant treatment advances; ongoing and future trials will demonstrate the degree to which we can improve on what we have achieved to date with pharmacologic treatments.
Am J Cardiol 2003 Mar 20
PMID:Improving clinical outcomes with drug treatment in heart failure: what have trials taught? 1267 Jun 37

This is the case report of a 13-year-old male who developed vasopressor-resistant hypotension after cardiac surgery for endocarditis. As norepinephrine resulted in aggravation of the preexisting ventricular arrhythmia, vasopressin was used to maintain blood pressure. The vasopressin continuous infusion was started at 0.00002 units/kg/min and titrated up to 0.0003 U/kg/min. This low dose led to resolution of hypotension without causing side effects. As the appropriate indication and dose of vasopressin is not established, the cautious use of vasopressin in children is recommended.
Pediatr Cardiol
PMID:Vasodilatory shock after surgery for aortic valve endocarditis: use of low-dose vasopressin. 1518 46

Severe right ventricular failure complicated a postoperative systemic inflammatory response in a 33-year-old woman after surgical repair of congenital cardiac malformations. Volume loading, and high doses of catecholamines, failed to produce improvement, but treatment with vasopressin improved all haemodynamic parameters, and also allowed reduction of the other inotropes. After 10 days, the patient was discharged in stable condition from the intensive care unit.
Cardiol Young 2005 Feb
PMID:The role of vasopressin in treating systemic inflammatory syndrome complicated by right ventricular failure. 1583 Nov 70

Vasoactive neurohormonal systems (eg, sympathetic nervous system [SNS], renin-angiotensin-aldosterone system, and arginine vasopressin [AVP]) are defense mechanisms designed to preserve arterial volume and circulatory homeostasis during periods of low cardiac output. Neurohormonal systems, which are normally stimulated under conditions of acute volume depletion, are activated by the low cardiac output and arterial pressure. However, sustained and chronic activation of these systems, as occurs in congestive heart failure (CHF), can cause progressive ventricular remodeling and worsening heart failure. Vasoconstriction, water retention, and increased blood volume are results of the activation of the SNS, the renin-angiotensin pathway, and AVP secretion. These effects can accelerate progression of CHF, contributing to increased morbidity and mortality. AVP regulates vascular tone and free-water reabsorption, respectively, through the vasopressin V(1a) and V(2) receptor subtypes and therefore is a potential neurohormonal target in the treatment of CHF.
Am J Cardiol 2005 May 02
PMID:Neurohormonal activation in congestive heart failure and the role of vasopressin. 1584 52

Hyponatremia in congestive heart failure (CHF) is associated with increased morbidity and mortality, underlining the importance of adequate assessment and treatment of this electrolyte imbalance in patients with CHF. Current treatment options for hyponatremia in CHF include hypertonic saline solution, loop diuretics, fluid restriction, and other pharmacologic agents, such as demeclocycline, lithium carbonate, and urea. Hypertonic saline solution must be administered with extreme caution because excessively slow or rapid sodium correction can lead to severe neurologic adverse effects. Loop diuretics are useful for reducing the water retention caused by CHF. However, the potent diuresis induced by agents such as furosemide results in loss of sodium and other essential electrolytes, which may exacerbate hyponatremia. Fluid restriction is only moderately effective and often difficult to implement in the hospital setting. Agents such as demeclocycline and lithium have potentially serious renal and cardiovascular side effects. The arginine vasopressin (AVP) receptor antagonists are a promising new class of aquaretic agents that increase free-water excretion while maintaining levels of sodium and other essential electrolytes. Tolvaptan (OPC-41061), lixivaptan (VPA-985), and conivaptan (YM-087) are currently under development for the treatment of hyponatremia. Although tolvaptan and lixivaptan are selective for the vasopressin-2 (V(2)) receptor responsible for the antidiuretic actions of AVP, conivaptan demonstrates activity at both the V(2) receptor and the V(1a) receptor responsible for the vasoconstricting properties of AVP. This dual receptor activity may be particularly useful in patients with CHF. These patients may benefit from the increased cardiac output, reduced total peripheral resistance, and reduced mean arterial blood pressure that results from V(1a) receptor blockade as well as the reduced congestion, reduced cardiac preload, and increased sodium concentrations induced by V(2) receptor antagonism.
Am J Cardiol 2005 May 02
PMID:Current treatments and novel pharmacologic treatments for hyponatremia in congestive heart failure. 1584 53

Current therapies for acute heart failure syndromes (AHFS) target hemodynamics by decreasing congestion or increasing myocardial contraction. Several new agents for AHFS use novel mechanisms of action that focus on new treatment targets, such as those providing anti-ischemic and anti-stunning effects, blocking vasopressin receptors, or blocking endothelin-1 receptors. For example, levosimendan acts as a calcium sensitizer and adenosine triphosphate-dependent potassium (K(ATP)) channel opener that increases contraction, causes vasodilation, and provides cardioprotective effects. This is accomplished by its dual mechanism of action. Levosimendan binds to cardiac troponin C, thereby enhancing calcium myofilament responsiveness and increasing myocardial contraction without increasing intracellular calcium levels. Thus, contraction is increased with no significant increase in myocardial oxygen consumption. The opening of K(ATP) channels by levosimendan causes vasodilation and exerts anti-ischemic and anti-stunning effects on the myocardium. Other new agents target neurohormonal pathways. Tezosentan is an antagonist of endothelin-1 receptors A and B. By inhibiting endothelin-1 receptors, tezosentan may counteract the activities of endothelin-1, which include vasoconstriction, proarrhythmic activities, potentiation of other neurohormones, and mediation of increased vascular permeability. Tolvaptan is a vasopressin V2-receptor antagonist that functions as an aquaretic (ie, it increases urine volume and serum sodium with little or no sodium loss). Therefore, by using novel mechanisms of action, these agents may provide new opportunities for helping patients with AHFS.
Am J Cardiol 2005 Sep 19
PMID:Pharmacology of new agents for acute heart failure syndromes. 1618 25

In a retrospective study of 36 patients who developed cardiogenic shock after myocardial infarction, intravenous vasopressin therapy increased mean arterial pressure from 56 to 73 mm Hg at 1 hour (p < 0.001) and maintained it for 24 hours without changing pulmonary capillary wedge pressure, cardiac index, urine output, or other inotropic requirements. After norepinephrine administration, mean pulmonary capillary wedge pressure increased at 1 hour from 21 to 24 mm Hg (p = 0.04); however, this increase was not sustained at 12 and 24 hours. Norepinephrine was associated with a significant increase in cardiac power index at 24 hours, whereas there was only a trend for an increase in cardiac power with vasopressin therapy. In a cohort of patients who developed refractory cardiogenic shock after myocardial infarction, vasopressin was associated with increased mean arterial pressure and no adverse effect on other hemodynamic parameters.
Am J Cardiol 2005 Dec 15
PMID:Effect of vasopressin on hemodynamics in patients with refractory cardiogenic shock complicating acute myocardial infarction. 1636 Mar 45


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