Home  About us  Contact
 

Vasopressin Receptor Antagonists (vasopressin + receptor_antagonist)

Distribution by Scientific Domains
Medical Sciences81%

Selected Abstracts

2,5-Disubstituted 3,4-Dihydro-2H-benzo[b][1,4]thiazepines as Potent and Selective V2 Arginine Vasopressin Receptor Antagonists.

CHEMINFORM, Issue 10 2004
Maud J. Urbanski
Abstract For Abstract see ChemInform Abstract in Full Text. [source]

Hyponatremia and Heart Failure,Treatment Considerations

CONGESTIVE HEART FAILURE, Issue 1 2006
Domenic A. Sica MD
Hyponatremia as it occurs in the heart failure patient is a multifactorial process. The presence of hyponatremia in the heart failure patient correlates with both the severity of the disease and its ultimate outcome. The therapeutic approach to the treatment of hyponatremia in heart failure has traditionally relied on attempts to improve cardiac function while at the same time limiting fluid intake. In more select circumstances, hypertonic saline, loop diuretics, and/or lithium or demeclocycline have been used. The latter two compounds act by retarding the antidiuretic effect of vasopressin but carry with their use the risk of serious renal and/or cardiovascular side effects. Alternatively, agents that selectively block the type 2 vasopressin receptor increase free water excretion without any of the adverse consequences of other therapies. Conivaptan, lixivaptan, and tolvaptan are three such aquaretic drugs. Vasopressin receptor antagonists will redefine the treatment of heart failure-related hyponatremia and may possibly evolve as adjunct therapies to loop diuretics in diuretic-resistant patients. [source]

Vasopressin receptor antagonists: pharmacological tools and potential therapeutic agents

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2006
J. O. Streefkerk
Summary 1 The present survey deals with the development and applications of non-peptidergic vasopressin receptor antagonists. 2 The existence of at least three vasopressin receptors (V1, V2 and V3 respectively) is firmly established. 3 V1 -receptors play a relevant role in the regulation of vascular tone, whereas V2 -receptors are known to mediate the antidiuretic activity of vasopressin at the level of the renal collecting ducts. The V3 -receptor appears to be involved in the release of the adreno-corticotropic hormone. 4 Vasopressin receptor antagonists which are peptides have been known for several decades, more recently, both V1 - and V2 -receptor blockers which are non-peptidergic have been introduced, as well as agents with affinity for both V1 - and V2 -receptor subtypes. A survey of these non-peptidergic antagonists is presented here. Such compounds are useful as pharmacological tools, and they can also be thought of as therapeutic agents as therapeutic agents in cardiovascular and renal diseases. 5 Selective V1 - and V2 -receptor antagonists were used to study the interaction between vasopressin receptors and sympathetic neurones. Depending on the experimental model used this interaction can occur at either the pre- or postsynaptic sites. In both cases predominantly V1 -receptors are involved. 6 A brief survey is given of the potential use of V-receptor antagonists in the drug therapy of syndrome of inappropriate antidiuretic hormone secretion and other water retaining disorders, congestive heart failure and certain forms of hypertension (in particular in the Negroid hypertensive patients). [source]

Hyponatremia and Vasopressin Antagonism in Congestive Heart Failure

CLINICAL CARDIOLOGY, Issue 11 2007
Siva Kumar M.D
Abstract In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists,agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia. Copyright © 2007 Wiley Periodicals, Inc. [source]

Peptide YY administration into the posterior hypothalamic nucleus of the rat evokes cardiovascular changes by non-adrenergic, non-cholinergic mechanisms

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2005
J. R. Martin
Summary 1 Microinjection of peptide YY (PYY) (0.23,2.3 nmol) into the posterior hypothalamic nucleus (PHN) of conscious rats evokes a dose-dependent pressor response and a bradycardia. 2 The increase in mean arterial pressure evoked by 2.3 nmol of PYY was not blocked by intravenous pretreatment with: (i) the nicotinic ganglionic receptor antagonist pentolinium (PENT, 10 mg kg,1) alone, or in combination with the muscarinic receptor antagonist methylatropine (MeATR, 1 mg kg,1); (ii) the ,1 -adrenoceptor antagonist prazosin (PRAZ, 0.2 mg kg,1); (iii) the V1 -vasopressin receptor antagonist [d(CH2)5Tyr(Me)]AVP (AVPX, 20 ,g kg,1); (iv) the combination of AVPX, PENT and MeATR; (v) the combination of PRAZ, AVPX, PENT, MeATR, and the ,2 -adrenoceptor antagonist yohimbine (0.3 mg kg,1); or (vi) the angiotensin II type 1 receptor antagonist ZD 7155 (1 mg kg,1). 3 Adrenal demedullation inhibited the PYY-evoked responses of drug-naïve rats, and rats pretreated with the combination of PENT, MeATR and AVPX. 4 Transection of the splanchnic nerve innervating the adrenal medullae attenuated the bradycardia, as did ZD 7155, but not the PYY-evoked pressor response. 5 Systemic pretreatment of rats with the neuropeptide Y1 receptor antagonist BIBP 3226 (1 mg kg,1) blocked the PYY-evoked cardiovascular changes, but not those evoked by microinjection of carbachol (5.5 nmol) into the PHN. 6 These results suggest that the cardiovascular changes evoked from the PHN by PYY requires the presence of the adrenal medullae, which are stimulated by: (i) a hormone to release an NPY-like substance that evokes the pressor response, and (ii) the splanchnic nerve to evoke the release of a substance that results in the bradycardia. [source]

Copeptin: A Biomarker of Cardiovascular and Renal Function

CONGESTIVE HEART FAILURE, Issue 2010
Nils G. Morgenthaler MD
Congest Heart Fail. 2010;16(4)(suppl 1):S37,S44. ©2010 Wiley Periodicals, Inc. Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists. [source]

Vasopressin receptor antagonism , a therapeutic option in heart failure and hypertension

EXPERIMENTAL PHYSIOLOGY, Issue 2000
Louise M. Burrell
The precise role of vasopressin in the pathophysiology of cardiovascular disease is controversial, but this peptide hormone is important for several reasons. Firstly, circulating concentrations of vasopressin are elevated in heart failure and some forms of hypertension. Secondly, there is evidence that vasopressin is synthesized not only in the hypophysial-pituitary axis but also in peripheral tissues including the heart where it acts as a paracrine hormone. Thirdly, vasopressin has vasoconstrictor, mitogenic, hyperplastic and renal fluid retaining properties which, by analogy with angiotensin II, may have deleterious effects when present in chronic excess. Finally, the availability of orally active non-peptide vasopressin receptor antagonists allows vasopressin receptor antagonism to be considered as a therapeutic option in cardiovascular disease. [source]

Vasopressin receptor antagonists: pharmacological tools and potential therapeutic agents

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2006
J. O. Streefkerk
Summary 1 The present survey deals with the development and applications of non-peptidergic vasopressin receptor antagonists. 2 The existence of at least three vasopressin receptors (V1, V2 and V3 respectively) is firmly established. 3 V1 -receptors play a relevant role in the regulation of vascular tone, whereas V2 -receptors are known to mediate the antidiuretic activity of vasopressin at the level of the renal collecting ducts. The V3 -receptor appears to be involved in the release of the adreno-corticotropic hormone. 4 Vasopressin receptor antagonists which are peptides have been known for several decades, more recently, both V1 - and V2 -receptor blockers which are non-peptidergic have been introduced, as well as agents with affinity for both V1 - and V2 -receptor subtypes. A survey of these non-peptidergic antagonists is presented here. Such compounds are useful as pharmacological tools, and they can also be thought of as therapeutic agents as therapeutic agents in cardiovascular and renal diseases. 5 Selective V1 - and V2 -receptor antagonists were used to study the interaction between vasopressin receptors and sympathetic neurones. Depending on the experimental model used this interaction can occur at either the pre- or postsynaptic sites. In both cases predominantly V1 -receptors are involved. 6 A brief survey is given of the potential use of V-receptor antagonists in the drug therapy of syndrome of inappropriate antidiuretic hormone secretion and other water retaining disorders, congestive heart failure and certain forms of hypertension (in particular in the Negroid hypertensive patients). [source]

Hyponatremia in Heart Failure: Revisiting Pathophysiology and Therapeutic Strategies

CLINICAL CARDIOLOGY, Issue 6 2010
Amir Kazory MD
Hyponatremia is frequently encountered in patients with heart failure (HF), and its association with adverse outcomes is well-established in this population. While hyponatremia is an independent marker for severity of HF, it is not certain whether it has a causal impact on the progression of the disease. There are no universally accepted consensus guidelines regarding therapeutic strategies for HF-associated hyponatremia and volume overload; current societal guidelines do not address management of this complication. Whereas thiazide diuretics are known to induce or worsen hyponatremia in this setting through a number of mechanisms, loop diuretics can be considered a readily available first-line pharmacologic therapy. Consistent with pathophysiology of the disease and mechanisms of action of loop diuretics, available clinical evidence supports such an approach provided that patients can be closely monitored. Use of vasopressin receptor antagonists is an emerging therapeutic strategy in this setting, and the efficacy of these agents has so far been shown in a number of clinical studies. These agents can be reserved for patients with HF in whom initial appropriate loop diuretic therapy fails to improve serum sodium levels. Copyright © 2010 Wiley Periodicals, Inc. [source]

Hyponatremia and Vasopressin Antagonism in Congestive Heart Failure

CLINICAL CARDIOLOGY, Issue 11 2007
Siva Kumar M.D
Abstract In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists,agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia. Copyright © 2007 Wiley Periodicals, Inc. [source]