◀ Back to ANGPT2

ANGPT2 — AVP

Text-mined interactions from Literome

Veltmar et al., J Pharmacol Exp Ther 1992 : 3 ) PVN mediated AVP release in response to periventricular ANG II-AT 1 receptor stimulation is at least partially effected through ANG II-AT 1 receptors in the PVN impinging on alpha adrenergic terminals
Reis et al., Exp Physiol 2007 : In contrast SNAP blocked the AVP , OT and ANP release, as well as antidiuretic and natriuretic responses induced by ANG-II
Schiavone et al., Proc Natl Acad Sci U S A 1988 : Ang II increased AVP release over the control value by 172 % +/- 44 % and 268 % +/- 66 % at 0.4 and 4 microM, respectively ; the same concentrations of Ang- ( 1-7 ) increased AVP release by 134 % +/- 12 % and 216 % +/- 45 % ... In the presence of the competitive Ang II antagonist [ Sar1,Thr8 ] Ang II ( 20 microM ), the release of AVP increased approximately equal to 2-fold
Qadri et al., J Pharmacol Exp Ther 1993 : In addition, ANG II AT1 receptors in the SON can contribute to AVP release after periventricular ANG II receptor stimulation
Salgado et al., Braz J Med Biol Res 1997 (Aortic Coarctation...) : Hormone assays carried out on blood collected from conscious rats submitted to aortic constriction supported a role for ANG II in the early stage and a combined role for both ANG II and AVP in the maintenance of proximal hypertension
Qadri et al., J Neuroendocrinol 1998 : ANG II ( 1-8 ) and the C-terminal ANG III ( 2-8 ) at 0.1-100 pmol/200 nl induced a dose dependent increase in AVP release with a maximum of 26.45+/-6.0 and 31.86+/-7.0 pg/ml, respectively, vs 1.6+/-2.0 pg/ml in vehicle treated controls ( P < 0.001 ) ... Our data demonstrate that the C-terminal ANG II ( 1-8 ) and ANG III ( 2-8 ), but not shorter fragments, can induce AVP release and drinking response via AT1 receptors in the PVN
Heitman et al., Am J Physiol 1998 (Anoxia) : Because plasma ANG II levels were lower during hypoxia and hypoxic release of arginine vasopressin from the pituitary into the plasma was prevented by ANG II receptor block, the brain renin-angiotensin system was likely involved
Mathai et al., Am J Physiol 1998 : Increases in arterial pressure, Na+ excretion, and plasma AVP concentration ([AVP]) in response to intracerebroventricular ANG II or intracerebroventricular 0.75 mol/l NaCl were either abolished or attenuated by intracerebroventricular infusion of losartan but not by intracerebroventricular infusion of artificial CSF or intravenous losartan