Disease relevance of Mcppa-avp

• Local blockade of endogenous AVP, d(CH2)5Tyr(Me)AVP (1 microgram-0.2 microliter), depressed baroreceptor reflex sensitivity with intense bradycardia to either small or large pressure increases [1].
• To assess the role of arginine vasopressin (AVP) in congestive heart failure (CHF), 10 patients with CHF refractory to conventional treatment were studied before and 60 minutes after intravenous administration of 5 micrograms/kg of d(CH2)5Tyr(Me)AVP, a specific antagonist of AVP at the vascular receptor level [2].
• AVP significantly potentiated the hypotension and the bradycardia produced by veratridine, whereas Manning compound blunted this potentiation [3].
• The sensitivity (slope) of the arterial baroreflex, as well as the reflex bradycardia induced by high blood pressure, increased significantly during AVP and returned to the control level after Manning compound [3].

High impact information on Mcppa-avp

• Furthermore, infusion of d(CH2)5Tyr(Me)AVP to water-deprived animals (n = 6) to antagonize endogenous AVP resulted in systemic but not renal vasodilation, so that kidney blood flow rate fell (by approximately 30%), as did systemic-to-renal resistance ratio (by approximately 30%) [4].
• In a first experiment, sexually inexperienced males received a single injection of AVP, saline, or d(CH2)5Tyr(Me)AVP in the lateral septum, after which their paternal responsiveness was recorded during a 10-min period [5].
• Moreover, a well-characterized V1 vasopressin antagonist, [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine]Arg8-vasopressin [d(CH2)5Tyr(Me)AVP], competes with [3H]AVP binding with an IC50 of 0.17 microM [6].
• Mean arterial pressure was reduced, and RSNA was increased by intravenous infusion of AVP antagonist d(CH2)5Tyr(Me)AVP (n = 8), whereas vertebral artery infusion of the antagonist (n = 6) did not change RSNA [7].
• The V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) had no effect on resting blood flow, but abolished the effect of vasopressin on blood flow to the choroid plexus [8].

Biological context of Mcppa-avp

• In renal-wrapped rats, ganglionic blockade caused a greater fall in blood pressure in animals treated with d(CH2)5Tyr(Me)AVP than in vehicle-treated animals [9].
• Metoclopramide pretreatment in urethane-anesthetized rats prevented the decreases in MAP and heart rate induced by LY171555, whereas pretreatment with d(CH2)5Tyr(Me)AVP delayed the recovery phase of the depressor response [10].
• Except for the pressor antagonist d(CH2)5Tyr(Me)AVP, this corresponds to their relative efficacy in displacing 3H-AVP from high-affinity specific binding sites on rat hippocampal synaptic membranes [11].
• AVP and related peptides reduced phosphorylation of this pre-synaptic phosphoprotein in the following order of potency: AVP = oxytocin greater than DG-AVP greater than dDAVP greater than d(CH2)5Tyr(Me)AVP = [pGlu4,Cyt6]AVP-(4-9) [11].
• A specific vasopressin vascular receptor antagonist, d(Ch2)5Tyr(Me)AVP, did not alter the baroreflex sensitivity in LE rats [12].

Anatomical context of Mcppa-avp

• In competition binding experiments with [3H]-SK&F 101926 using cell and liver membranes, guanosine 5'-(beta,gamma-imido)triphosphate did not significantly alter the affinity of the V1 antagonist d(CH2)5Tyr(Me)AVP, but the affinity of AVP was decreased [13].
• However, when the vasopressin V1 antagonist, d(CH2)5Tyr(Me)AVP, was injected into the ventral septal area prior to interleukin-1, a fever was evoked which was significantly greater in magnitude and duration [14].
• In a subsequent experiment we investigated the physiological impact of the stressor-induced release of AVP by administrating the AVP V1 receptor antagonist d(CH2)5Tyr(Me)AVP into the amygdala via inverse microdialysis [15].
• Two days later, they were trained on 3 consecutive days (12 daily trials) to locate the hidden underwater platform in the Morris water maze (MWM) while the probes were perfused with either artificial cerebrospinal fluid (aCSF) or aCSF containing vasopressin or the V1 antagonist d(CH2)5Tyr(Me)AVP (AAVP) [16].
• Distinct mechanisms of action of V1 antagonists OPC-21268 and [d(CH2)5Tyr(Me)AVP] in mesangial cells [17].

Associations of Mcppa-avp with other chemical compounds

• In LE rats, however, i.v. pretreatment with the specific vascular antagonist to the pressor effect of AVP, d(CH2)5Tyr(Me)AVP (VP-ANT; 10 micrograms/kg), significantly attenuated, but did not completely block the hypertensive and bradycardic effects of i.c.v. methoxamine and phenylephrine.(ABSTRACT TRUNCATED AT 250 WORDS)[18]
• The vasopressor antagonist of arginine vasopressin (AVP), d(CH2)5Tyr(Me)AVP (10 micrograms/kg i.v.) and phenoxybenzamine (1 mg/kg i.v.) partly blocked and hexamethonium (25 mg/kg i.v.) enhanced the pressor action of LY171555 [19].
• SR 49059 was even about six times more efficient than d(CH2)5Tyr(Me)AVP in inhibiting AVP-induced DNA synthesis [20].
• Aggression by territorial males towards 'intruders' (bottled fishes) was assessed before and after each male received intramuscular injections of either AVT, Manning compound (an AVT V1a receptor antagonist), isotocin (the teleost homologue of mammalian oxytocin differing from AVT by two amino acids) or saline (vehicle control) [21].
• The pressor effects of ET-1 were reduced by diltiazem, nitrendipine, verapamil or cromakalim and unchanged after BW 755c, desipramine, enalapril, indomethacin, methysergide, phentolamine or SK&F 100273 [22].

Gene context of Mcppa-avp

• The binding sites were specific and saturable: studies with the V1 AVP antagonist d(CH2)5Tyr(Me)AVP and the V2 agonist 1-deamino-8-D-AVP indicated that the AVP receptor was V1 in specificity [23].
• The selective vascular (V1) receptor antagonist [d(CH2)5 1Tyr(Me)2]AVP (SK&F 100273) shifted the concentration-response curves for AVP-induced vascular contraction to the right in a parallel manner (KB = 2.23 X 10(-9) M) [24].
• The enhanced cardiovascular effects of AVP in OT-pretreated animals were dose dependent, blocked by the V1 antagonist d(CH2)5Tyr(Me)AVP, not evoked by OT alone, and occurred in the absence of changes in basal (nonstimulated) MAP and HR [25].
• Displacement of 3H-AVP binding with high affinity by unlabelled AVP, LVP and the V1 antagonist, d(CH2)5Tyr(Me)AVP, indicated that the Leydig cell AVP receptor is of the V1 type [26].
• The potentiation by vasopressin was reduced by the antagonist of vasopressin V1 receptors d(CH2)5Tyr(Me)AVP (10(-7) M), but not by the vasopressin V2 receptor antagonist d(CH2)5D-Ile2, Ile4AVP (10(-7) M) [27].

Analytical, diagnostic and therapeutic context of Mcppa-avp

• In a second experiment, the introduction of the V1 receptor antagonist d(CH2)5Tyr(Me)AVP into the mediolateral septum via inverse microdialysis concomitant with stressor exposure caused the rats to spend an increased time floating and a reduced time swimming compared to vehicle-treated rats [28].
• DPTyr(Me)AVP was microinjected into the anterior hypothalamus 1 h before the microinjection of AVP while d(CH2)5Tyr(Me)AVP and AVP were prepared together and delivered as a single microinjection [29].
• Intravenous injection of the V1 antagonist, d(CH2)5Tyr(Me)AVP, significantly reduced the elevated mean arterial pressure induced by 50 or 100 ng/h of AVP (-7 +/- 4 and -11 +/- 2 mmHg, respectively) [30].
• Despite the slight sauna-induced elevation in circulating vasopressin, intravenous injection of the specific vascular vasopressin antagonist d(CH2)5Tyr(Me)AVP (5 micrograms/kg) 1 h after the sauna had no effect on blood pressure, heart rate or skin blood flow [31].

References