Vasopressin: Applications in Clinical Practice

Dyke, Peter C.; Tobias, Joseph D.

doi:10.1177/0885066604265246

Cited by 19 publications

(17 citation statements)

References 37 publications

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“…Its main physiological function is to regulate the volume of body fluid. With its proven pressor effect on blood vessels by targetingV 1A R, it is presently used to manage cardiac arrest in adults and vasodilatory shock in children . The concentration of AVP in the circulation is <1.6 × 10 −12 mol/L in a healthy adult, but plasma levels of AVP in patients with chronic heart failure may rise to 2.5‐6.4 × 10 −12 mol/L .…”

Section: Discussionmentioning

confidence: 99%

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

Chen

Zhang

et al. 2017

Clin Exp Pharma Physio

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Cardiac fibrosis is a pathological feature commonly found in hearts exposed to haemodynamic orneurohormonal stress. Elevated levels of arginine vasopressin (AVP) are closely associated with the progression of heart failure and could be an underlying cause of cardiac fibrosis. The aim of this study is to characterize the effect of AVP on neonatal rat cardiac fibroblasts (NRCFs) and to illustrate its signalling mechanism. The proliferative effect of AVP was assessed by methylthiazolyldiphenyl-tetrazolium assay and 5-bromo-2'-deoxyuridine (BrdU) incorporation assay, and the amounts of cellular signalling proteins α-smooth muscle actin (α-SMA), matrix metalloproteinase (MMP) 2, MMP9, and phosphorylated ERK were determined by western blotting. AVP, in a time- and concentration-dependent manner, promoted NRCF proliferation and the expression of MMP2 and MMP9. Inhibition of G protein-coupled receptor kinase2 (GRK2) by the inhibitory peptide GRK2-Ct or knock-down of GRK2 suppressed AVP-induced BrdU incorporation and the expression of MMP2 and α-SMA in NRCFs. Moreover, shRNA-mediated silencing of β-arrestin1 or β-arrestin 2 abolished AVP-induced BrdU incorporation and MMP2 expression. AVP-induced NRCF proliferation depended on the phosphorylation of ERK , and inhibition of GRK2 or silencing of β-arrestins blocked AVP-induced ERK phosphorylation. The effects of AVP on NRCF proliferation and α-SMA expression were blocked by SR45059, a vasopressin receptor type1A (V R) selective antagonist. In conclusion, AVP promotes NRCF proliferation through V R-mediated GRK2/β-arrestin/ERK signalling.

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Section: Discussionmentioning

confidence: 99%

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

Chen

Zhang

et al. 2017

Clin Exp Pharma Physio

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“…Daþniausiai vartojami vazopresoriai -katecholaminai. Ligoniai, kuriø jautrumas katecholamininiams vazopresoriams sumaþëjaes, pvz., dël tachifilaksijos, gydomi didesnëmis jø dozëmis, todël dël katecholaminø toksiðkumo padidëja nepageidaujamø reiðkiniø (1,5). Mirðtamumas didelis, o alternatyvø nedaug (6).…”

Section: áVadasunclassified

“…1898 m. pateikti duomenys apie hipofizës ekstrakto vazokonstrikciná poveiká. 1951 m. paskelbta apie iðskirtà ið hipofizës arginino vazopresinà, o pirmasis jo sintetinis preparatas sukurtas 1954 m. Arginino vazopresinas klinikinëje praktikoje pradëtas vartoti 1955 m. necukriniam diabetui gydyti, ir tai beveik pusae amþiaus buvo vienintelë jo vartojimo sritis (5,7).…”

Section: Vazopresino Struktûra Sintezës Vieta Ir Iðsiskyrimasunclassified

“…V1R, kurie dar vadinami V1a receptoriais, aptinkami kraujagysliø lygiuosiuose raumenyse, taip pat ðirdies miocituose, smegenyse, sëklidëse, virðutiniuose simpatiniuose kaklo mazguose, kepenyse, inkstø ðerdyje, trombocituose. Stimuliuojant V1R, skatinamas vidulàstelinës kalcio jonø koncentracijos didëjimas susidarant inozitoltrifosfatui (IP 3 ), todël vyksta vazokonstrikcija, trombocitø agregacija (5,7).…”

Section: Vazopresino Receptoriai Ir Veikimasunclassified

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Vasopressin for treatment of hemodynamic disorders

Adukauskienė¹,

Širvinskas²,

Kėvelaitis³

2008

Medicina

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Vasopressin is a 9-amino acid peptide synthesized by magnocellular neurons of the hypothalamus and released from posterior pituitary gland. The primary physiological role of vasopressin is the maintenance of fluid homeostasis. In this review, the classification of vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary, oxytocin receptors, and purinergic receptors, and the effects of vasopressin on vascular smooth muscles, the heart, and the kidneys are discussed. Mortality rates of vasodilatory (or distributive), for example septic shock, are high. The use of vasopressin is an alternative therapy for vasodilatory shock with better outcome. Vasopressin is effective in resuscitation of adults after ventricular fibrillation or pulseless tachycardia, when epinephrine is not effective.

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“…Vasopressin mediates vasoconstriction through the activation of V-1 receptors in vascular smooth muscle cells and exerts its antidiuretic effect via activation of the V-2 receptor in the renal collecting ducts [2]. The activation of V-1 receptors causes elevation of the concentration of cytoplasmic free calcium whereas the activation of V-2 receptors produces a rise of cyclic AMP levels due to the stimulation of adenylate cyclase [2].…”

Section: Introductionmentioning

confidence: 99%

Vasopressin acts on platelets to generate procoagulant activity

Tomasiak

Stelmach²,

Rusak³

et al. 2008

Blood Coagulation &Amp; Fibrinolysis

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The aim of our study was to examine whether arginine vasopressin (AVP) is able to evoke in human platelets a procoagulant response due to activation of an Na+/H+ exchanger. It was found that treatment of platelets with AVP (20-100 nmol/l) results in generation of a weak calcium signal, activation of Na+/H+ exchanger, aggregation, and development of a procoagulant response. The AVP-evoked procoagulant response was dose and time dependent, weaker than that produced by collagen or monensin (mimics Na+/H+ exchanger), and less pronounced following the inhibition of Na+/H+ exchanger by 5-(N-ethyl-N-isopropyl) amiloride or genistein. Flow cytometry studies reveal that in-vitro platelet treatment with AVP results in an unimodal left shift in the forward and side scatter of the entire platelet population, indicating morphological changes on the plasma membrane. The shift was dose related, weaker than that evoked by collagen, similar to that produced by monensin and strongly reduced in the presence of 5-(N-ethyl-N-isopropyl) amiloride or genistein. Using flow cytometry, we demonstrated enhanced expression of phosphatidylserine on the AVP-treated platelets. AVP-evoked phosphatidylserine exposure was dose dependent, inhibited by 5-(N-ethyl-N-isopropyl) amiloride or genistein and weaker than that produced by collagen. AVP in a dose-dependent manner produced a rise in platelet volume. The swelling was inhibited by 5-(N-ethyl-N-isopropyl) amiloride, and its kinetics was similar to that observed in the presence of monensin. We conclude that prolonged treatment of platelets with AVP results in a procoagulant response, which may occur as a consequence of Na+ influx mediated by Na+/H+ exchanger.

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Vasopressin: Applications in Clinical Practice

Cited by 19 publications

References 37 publications

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

Vasopressin for treatment of hemodynamic disorders

Vasopressin acts on platelets to generate procoagulant activity

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