Disease relevance of Avpi1

• Arginine vasopressin-induced hypertrophy of cultured rat aortic smooth muscle cells [1].
• We previously reported that pertussis toxin (PTX) had little effect on arginine vasopressin-induced formation of inositol trisphosphate (IP3) in rat aortic smooth muscle cells [Kondo et al.: Biochemical and Biophysical Research Communications 161:677-682, 1989] [2].
• CONCLUSION: These findings suggest that neural modulation of arginine vasopressin-induced hypertension is altered during pregnancy and are consistent with a reduction in intrinsic vascular sensitivity to arginine vasopressin during gestation [3].

Psychiatry related information on Avpi1

• Arginine vasopressin induced persistent maternal behavior, but this behavior had a later onset [4].

High impact information on Avpi1

• Arginine vasopressin-induced [Ca2+]i responses in A10 rat vascular myocytes were therefore studied in vitro [5].
• Exposure of the elongated SMCs to endothelin 1, alpha-thrombin, or arginine vasopressin induced elevations in [Ca2+]i and [Na+]i and membrane depolarization [6].
• Mechanisms of angiotensin II- and arginine vasopressin-induced increases in protein synthesis and content in cultured rat aortic smooth muscle cells. Evidence for selective increases in smooth muscle isoactin expression [7].
• Identification of calcium-independent phospholipase A2 (iPLA2) beta, and not iPLA2gamma, as the mediator of arginine vasopressin-induced arachidonic acid release in A-10 smooth muscle cells. Enantioselective mechanism-based discrimination of mammalian iPLA2s [8].
• The increase in cell surface B2 receptors were functionally coupled to an increase in phosphoinositide-specific phospholipase C, and the effects of PDGF were selective as there was no increase in either angiotensin II- or arginine vasopressin-induced inositol phosphate formation or intracellular calcium release [9].

Biological context of Avpi1

• As a result, 19 demonstrated antagonist activities toward an arginine vasopressin-induced increase in diastolic blood pressure after intravenous or oral administration and long-lasting oral activity [10].
• Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors [11].
• Oxytocin pretreatment enhances arginine vasopressin-induced motor disturbances and arginine vasopressin-induced phosphoinositol hydrolysis in rat septum: a cross-sensitization phenomenon [12].
• Arginine vasopressin-induced renal vasodilation mediated by nitric oxide [13].
• 1. Epidermal growth factor is a potent mitogen that causes natriuresis, diuresis and inhibition of arginine vasopressin-induced water reabsorption [14].

Anatomical context of Avpi1

• These findings therefore indicate that the arginine vasopressin-induced increase in intracellular sodium concentration is augmented in vascular smooth muscle cells of SHR mediated through the enhancement of the mobilization of cytosolic free calcium and the activity of sodium-hydrogen exchange, which depends on an increase in V1 receptor number [15].
• Effects of N-ethylmaleimide on arginine vasopressin-induced responses in an established smooth muscle cell line [16].
• The presence of 12-O-tetradecanoylphorbol 13-acetate markedly decreased arginine-vasopressin-induced [3H]thymidine incorporation in fibroblasts from spontaneously hypertensive rats and was without effect in fibroblasts from Wistar-Kyoto rats [17].
• Glucose dependency of arginine vasopressin-induced insulin and glucagon release from the perfused rat pancreas [18].
• Arginine vasopressin induced motor disturbances in the medial amygdala: evidence for the involvement of a V1-type of AVP receptor [19].

Associations of Avpi1 with chemical compounds

• Cyclosporine A (10 micrograms/ml) did not affect resting intracellular free Ca2+ ([Ca2+]i) levels (151 +/- 10 vs. 146 +/- 5 nM, NS), but augmented the 10(-8) M arginine vasopressin-induced increase of [Ca2+]i (delta 76 +/- 4 vs. delta 172 +/- 6 nM, p less than 0.001) [20].
• Pretreatment of both cell groups with a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, completely blocked arginine vasopressin-induced intracellular alkalinization and increased intracellular sodium concentration [15].
• Prompt inhibition of arginine vasopressin-induced cellular adenosine 3',5'-monophosphate production by extracellular sodium depletion in rat renal inner medullary collecting duct cells in culture [21].
• Serotonin and adrenocorticotropin (ACTH) release: direct effects at the anterior pituitary level and potentiation of arginine vasopressin-induced ACTH release [22].
• CONCLUSION: The incorporation of eicosapentaenoic acid or linoleic acid at the sn-2 position of membrane phospholipids leads to an inhibition of arginine vasopressin-induced formation of diradylglycerols or phosphatidic acid, respectively, in rat mesenteric artery vascular smooth muscle cells in culture [23].

Other interactions of Avpi1

• Oxytocin at physiological concentrations evokes adrenocorticotropin (ACTH) release from corticotrophs by increasing intracellular free calcium mobilized mainly from intracellular stores. Oxytocin displays synergistic or additive effects on ACTH-releasing factor or arginine vasopressin-induced ACTH secretion, respectively [24].
• Cellubrevin, therefore, is in a position to mediate one or more steps in arginine vasopressin-induced water channel cycling [25].
• Biphasic effect of interleukin-1 beta on arginine vasopressin-induced cellular cyclic adenosine monophosphate production in cultured rat renal papillary collecting tubule cells [26].
• ZTTA, a prolyl endopeptidase inhibitor, potentiates the arginine-vasopressin-induced incorporation of [14C]leucine in rat amygdaloid and cortical slices [27].
• This vasopressor antagonist appears to be selective for arginine-vasopressin-induced motor disturbances, in that the convulsive and motor effects of pentylenetetrazol and somatostatin were not altered significantly by pretreatment with the central antagonist [28].

Analytical, diagnostic and therapeutic context of Avpi1

• Arginine vasopressin-induced increases in [35S]methionine incorporation was increased within 6 hours after treatment [1].

References