UNIPROT:P01185 - FACTA Search

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)

During the last years, the results of several trials on heart failure treatment were published or presented at international meetings. The new perspectives concern drug therapy and non-pharmacological strategies, such as cardioverter-defibrillators, biventricular resynchronization and implantable assist devices. Trials on beta-blockers extended the indication to patients with advanced heart failure, but the choice of the "best" beta-blocker to use remains an unsolved issue. Moreover, the concomitant use of ACE-inhibitors and angiotensin II receptor antagonists is a recent acquisition. However, the Val-HeFT results underscored that the add-on hypothesis of a more complete inhibition obtained with the combination of multiple agents was not confirmed in patients already taking ACE-inhibitors and beta-blockers. Regarding the new neurohormonal modulators (omapatrilat, etanercept, endothelin receptor blockers, arginine-vasopressin antagonists), more data are needed before using them in clinical practice. After the publication of the MADIT-II results, the cardioverter-defibrillator implantation will probably spread in patients with previous myocardial infarction and left ventricular dysfunction to prevent sudden death, but the cost-effectiveness ratio is still to be clarified. In the advanced or end-stage heart failure, when the improvement of quality of life represents the main target of therapy, ventricular resynchronization and implantable assist devices may play a role in clinical settings. Before considering them like a real therapeutic option, final results from ongoing investigations should be awaited.
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PMID:[Treatment of heart failure: an update]. 1218 29

Previous in vivo studies in cardiomyopathic hamsters suggested that the expression of vasopressin (AVP) V2 mRNA is up- regulated by angiotensin II. The present study was performed to determine whether angiotensin II plays a role in regulating the expression of AVP V2 mRNA and aquaporin-2 (AQP2) mRNA in the inner medullary collecting duct (IMCD) of the male Wistar rat. The expression of AVP V2 mRNA and AQP2 mRNA in the IMCD was measured by competitive reverse-transcriptase polymerase chain reaction (RT-PCR). Six groups of experiments were performed. In the first group, we incubated IMCD with 3 different doses of angiotensin II (10(-11), 10(-9) and 10(-7) mol/L). Angiotensin II caused a significant increase in the AVP V2 mRNA in a dose-dependent manner but its effect on AQP2 mRNA was modest. This effect of angiotensin II was inhibited by angiotensin II receptor antagonist, [Sar1,Ile8]-angiotensin II. To examine the role of PKA in mediating an increase in AVP V2 mRNA expression, we incubated IMCD with 10(-7) and 10(-11) M of angiotensin II in the presence of a specific protein kinase A (PKA) inhibitor, Rp diasteroisomer of adenosine 3'-5'-cylic monophosphothionate (Rp-cAMPS). The angiotensin II-induced upregulation of V2 mRNA was abolished. In the fourth group, we examined the effect of protein kinase C (PKC) inhibition on V2 mRNA expression. The upregulation of V2 mRNA induced by angiotensin II was greatly exaggerated when IMCD was incubated with angiotensin II and RO-31-8220 (PKC inhibitor). In the fifth and sixth groups of studies, we determined the direct effect of PKA and PKC on regulating the expression of V2 mRNA and AQP2 mRNA in the IMCD, respectively. Dibutryl cAMP stimulated an upregulation in the expression of V2 mRNA and AQP2 mRNA, whereas phorbol esters suppressed the expression of V2 mRNA. These results suggested that PKA stimulates and PKC suppresses the expression of V2 mRNA in the IMCD of the kidney.
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PMID:Angiotensin II upregulates the expression of vasopressin V2 mRNA in the inner medullary collecting duct of the rat. 1264 65

Hypertension is a very common condition and the most important risk factor for the occurrence of cardiovascular events. The hyperactivity of the renin-angiotensin-aldosterone system is considered a cardiovascular risk factor in subjects with essential hypertension. The intrinsic vascular abnormality in which the renin-angiotensin-aldosterone system is clearly the milieu for the development of the pathologic changes in blood vessel walls is one of the causes of the establishment of hypertension. Many drugs with different mechanisms of action have been used for the treatment of hypertension and its vascular complications. Nevertheless, the utilities of many drugs are limited by their adverse effects. Continuous research in the search for new pharmacological agents for the treatment of hypertension has led to the development of angiotensin II receptor type AT1 blockers. The most important functions mediated by AT1 receptors include: vasoconstriction, induction of the production and release of aldosterone, renal reabsorption of sodium, cardiac cellular growth, proliferation of vascular smooth muscle, increase of peripheral noradrenergic action and the central activity of the sympathetic nervous system, stimulation of vasopressin release, and inhibition of renin release from the kidney. The angiotensin II receptor type AT1 blockers inhibit the interaction of angiotensin II with its AT1 receptor. These agents lower blood pressure without producing cough as a side effect since, unlike the angiotensin-converting enzyme inhibitors they do not influence the levels of bradykinin or substance P. Hence, these drugs are suitable for the treatment of hypertensive patients who require therapy with a drug blocking the effect of angiotensin-converting enzyme but cannot use angiotensin-converting enzyme inhibitors due to cough as a side effect.
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PMID:Role of angiotensin II AT1 receptor blockers in the treatment of arterial hypertension. 1462 77

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.
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PMID:Congestive heart failure: what should be the initial therapy and why? 1472 93

In the present study, we investigated the cardiovascular effects of centrally injected U-46619, a thromboxane A(2) (TXA(2)) analog, and the central and peripheral mechanisms of these effects in hemorrhagic shock conditions. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood/100 g body weight over a period of 10 min. Injections were made into the lateral cerebral ventricle (LCV), nucleus tractus solitarius (NTS), rostral ventrolateral medulla (RVLM) and paraventricular nucleus of hypothalamus (PVN). U-46619 (0.1, 1 and 2 microg) increased blood pressure and reversed hypotension in hemorrhagic shock. The pressor effect was dose- and time-dependent in all investigated brain areas. Heart rate changes were not significantly different in all groups. Pretreatment of rats with an injection of SQ-29548 (4 or 8 microg), a TXA(2) receptor antagonist, into the LCV, NTS, RVLM and PVN completely blocked the pressor effect of U-46619 (1 microg) injected into respective brain areas. Hemorrhage itself increased plasma adrenaline, noradrenaline, vasopressIN levels and renin activity. U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS produced additional increases in these hormone levels and in renin activity. Intravenous pretreatments of rats with prazosin (0.5 mg/kg), an alpha(1)-adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2),Arg(8)]- vasopressin (10 microg/kg), a vasopressin V(1)-receptor antagonist, or saralasin (250 microg/kg), an angiotensin II receptor antagonist, in hemorrhaged rats partially blocked the pressor response to U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS. Results show that centrally administered U-46619, a TXA(2) analog, increases blood pressure and reverses hypotension in hemorrhagic shock. Activation of central TXA(2) receptors mediates the pressor effect of the drug. Furthermore, the increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity are involved in these effects.
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PMID:Restoration of blood pressure by centrally injected U-46619, a thromboxane A(2) analog, in hemorrhaged hypotensive rats: investigation of different brain areas. 1500 18

In this study we investigated the influence of d(CH2)5-Tyr(Me)-[Arg8]vasopressin (AAVP) and [adamanteanacetyl1,0-ET-d-Tyr2,Val4,aminobutyryl6,Arg8,9]-[Arg8]vasopressin (ATAVP), which are antagonists of vasopressin V1 and V2 receptors, and the effects of losartan, a selective angiotensin AT1 receptor antagonist, and CGP42112A, a selective AT2 receptor antagonist, injected into the lateral septal area (LSA) on thirst and hypertension induced by [Arg8]vasopressin (AVP). AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT1 and AT2 ligands administered into the LSA elicited a concentration-dependent decrease in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of AAVP from 18 +/- 1 to 6 +/- 1 mm Hg. Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 +/- 0.8 mm Hg. ATAVP and CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT1 receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple AVP and angiotensin II receptor subtypes. The pressor response of AVP was reduced by losartan and by AAVP. CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of V1 receptors and that the inhibitory effect requires V2 receptors. The involvement of AT1 and AT2 receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance.
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PMID:Influence of arginine vasopressin receptors and angiotensin receptor subtypes on the water intake and arterial blood pressure induced by vasopressin injected into the lateral septal area of the rat. 1510 40

A 66-year-old woman treated with valsartan, an angiotensin II receptor blocker, and diuretics was scheduled for surgery to remove a pelvic mass. Both drugs were withdrawn 24 hours before anesthetic induction. Combined general and epidural anesthesia was provided. When hypotension developed and was refractory to fluid replacement and phenylephrine administration, terlipressin, a vasopressin receptor antagonist, was infused and outcome was favorable. Anesthetized patients treated with angiotensin II receptor blockers to control hypertension may experience hypotensive events that are refractory to standard treatment but that respond to vasopressin receptor antagonists.
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PMID:[Refractory hypotension during anesthesia in a patient treated with angiotensin receptor blockers]. 1530 35

Bilateral carotid occlusion (BCO) increases the sympathetic drive to the circulatory system in conscious intact rats, producing a hypertensive response characterized by two components, i.e., an initial peak followed by a sustained response of lower intensity. The neurohumoral mechanisms involved in the hypertensive response to BCO were evaluated in conscious intact (INTACT) or chronic guanethidine sympathectomized (SYMPX) rats. To accomplish this, the receptor antagonists, prazosin for alpha1-adrenergic receptor, losartan for AT1 angiotensin II receptor and [d(CH2)5Tyr(Me)AVP] for vascular V1 vasopressin receptor were used. A saline control group was studied as well. Conscious rats were equipped with cuffs around the common carotid arteries plus arterial and venous catheters. The results indicate that the sympathetic nervous system is the main mechanism controlling the basal arterial pressure in conscious INTACT rats, whereas in chronically SYMPX rats the renin-angiotensin system plays this role. In INTACT rats prazosin abolished the initial peak and blunted the sustained hypertensive response due to BCO, while the other antagonists exhibited no effect. SYMPX rats did not present the initial peak but displayed an enhanced sustained response, which was blunted by prazosin or the vasopressin antagonist. In conclusion, activation of the sympathetic drive is responsible for both the initial peak and the sustained hypertensive response due to BCO in conscious INTACT rats. On the other hand, vasopressin acting in concert with the sympathetic nervous system, plays a key role in the potentiation of the sustained hypertensive response due to BCO in conscious chronically SYMPX rats.
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PMID:Neurohumoral mechanisms involved in the hypertensive response elicited by bilateral carotid occlusion in conscious intact or chronically sympathectomized rats. 1555 56

The purpose was to apply oxidative crosslinking reactions to the study of recognition and signaling mechanisms associated to G-protein-coupled receptors. Using a ruthenium chelate, Ru(bipy)(3)(2+), as photosensitizer and visible light irradiation, in the presence of ammonium persulfate, we performed fast and efficient covalent labeling of the B(2) bradykinin receptor by agonist or antagonist ligands possessing a radio-iodinated phenol moiety. The chemical and topographical specificities of these crosslinking experiments were investigated. The strategy could also be applied to the covalent labeling of the B(1) bradykinin receptor, the AT(1) angiotensin II receptor, the V(1a) vasopressin receptor and the oxytocin receptor. Interestingly, we demonstrated the possibility to covalently label the AT(1) and B(2) receptors with functionalized ligands. The potential applications of metal-chelate chemistry to receptor structural and signaling studies through intramolecular or intermolecular crosslinking are presented.
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PMID:Crosslinking photosensitized by a ruthenium chelate as a tool for labeling and topographical studies of G-protein-coupled receptors. 1566 11

The two main causes of cardiac edema are congestive heart failure and pericardial diseases. Careful evaluation of patients with edema is important because there are many other diseases showing the symptom. Important for the treatment of edema is to restrict sodium and water intake. Diuretics and digoxin have formed the mainstay of treatment for many years. Patients with edema should be given diuretics until an euvolemic state is achieved. Especially loop diuretic is effective to reduce edema quickly. Recently atrial natriuretic peptide and brain natriuretic peptide are shown to be useful markers to assess heart failure. These peptides are also useful as therapeutic tools for treating edema in heart failure. Even if the patient has responded favorably to diuretics, angiotensin converting enzymes inhibitors, angiotensin II receptor blockers, beta blockers and spironolactone should be added according to the status, because there are many evidences that they improve the long-term prognosis. Vasopeptidase inhibitors and vasopressin antagonist are being introduced for management of heart failure.
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PMID:[Edema in heart disease]. 1567 20

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