Disease relevance of AVP

• These results demonstrate that the enhanced release of AVP during hemorrhage with ANS blockade can be mediated either by cardiac or arterial baroreceptors; however, the maximum response is elicited only when both sets of receptors are functioning normally [1].
• In summary, NHX attenuated the ACTH response to hypotension (large peripheral AVP response) but not to INS or CRF (small peripheral AVP response).(ABSTRACT TRUNCATED AT 250 WORDS)[2]
• AVP infusion restored renal blood flow and Do2 in endotoxic shock compared with animals resuscitated with NE, which had persistently low renal blood flow and Do2 [3].
• Chronic chloride depletion alkalosis in dogs causes a lowered osmotic threshold and increased sensitivity for vasopressin (AVP) release [4].
• CRH, AVP, IGF-I and cortisol had no effect on the proliferation of canine pituitary cells or canine corticotrophic adenoma cells [5].

Psychiatry related information on AVP

• Since AVP release and drinking behavior normally are closely associated over a narrow range of changes in plasma osmolality (Posm), we investigated whether alkalotic dogs would also show an altered responsiveness to the dipsogenic effects of angiotensin II (ANG II) and osmotic stimuli [4].

High impact information on 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 [6].
• Treatment with either 10 microM CPA or 1 mM ATP also caused an increase in UT-A2-mediated urea flux, although these responses where transient compared with those induced by AVP or elevated cAMP [7].
• We found that AVP decreased the lumen diameter of microperfused afferent arterioles dose-dependently and that a V1 antagonist, OPC21268, inhibited the vasoconstrictor action of AVP [8].
• We have previously reported that vasopressin (AVP) V2 receptor stimulation increased renal blood flow in dogs anesthetized with pentobarbital [8].
• These results suggest that AVP V2 receptors are present in rabbit afferent arterioles and that V2 receptor stimulation induces vasodilation in rabbit afferent arterioles [8].

Chemical compound and disease context of AVP

• The effects of intravenous norepinephrine (NE, group 1) and vasopressin (AVP, group 2) infusions on systemic, splanchnic, and renal circulations were studied in anesthetized dogs under basal conditions and during endotoxic shock [3].
• Initial hemorrhage led to a small but significant increase in adrenal cortisol secretion and circulating ACTH, vasopressin (AVP), angiotensin II (AII), and plasma renin activity (PRA) [9].
• To study responses of methionine enkephalin-like substance (MELS) and vasopressin (AVP) to hemorrhage, plasma MELS, AVP, and catecholamine levels and mean arterial blood pressure (MAP) and central venous pressure (CVP) were investigated in intact and adrenalectomized dogs (n = 34) under pentobarbital anesthesia [10].
• We examined the interaction of graded hypoxia and hypercapnia on stimulation of vasopressin (AVP), ACTH, and corticosteroids in nonsurgically stressed, pentobarbital-anesthetized, gallamine-paralyzed ventilated dogs [11].

Biological context of AVP

• Barium, in the presence of AVP and IBMX, depolarized the cell membrane potential (bis-oxonol fluorescence increased 22.3 +/- 0.03%), reversed secretion to absorption (from 3.21 +/- 0.93 to -1.52 +/- 0.61 x 10(-6) ml/min/cm2), and increased cell volume 2.7 +/- 0.5% [12].
• In the absence of AVP and IBMX bumetanide had no effect on fluid transport, cell volume or membrane potentials [12].
• SAP stimulation or AVP stimulation selectively decreased heart rate or increased atrioventricular conduction time, respectively [13].
• The data demonstrate that opiate receptors behind the BBB are primarily involved in kappa agonist-induced water diuresis and possibly inhibition of AVP secretion [14].
• The time to maximal ankle venous pressure after standing (VFT) and to 90% of that time after exercise (VRT90), and the minimal pressure after exercise (AVP) were measured in 17 greyhounds before intervention, after only the superficial femoral vein valve remained (n = 5), and after complete lower limb venous valvulotomy (n = 17) [15].

Anatomical context of AVP

• Distension of the left atrium led within 2 min to a fall in plasma AVP concentration which reached a steady lower value within 4 min [16].
• However, median eminence staining for AVP and neurophysin was greatly diminished in neurohypox dogs [17].
• Immediately after single superficial femoral vein valve construction, VFT, AVP, and VRT90 measurements were not significantly different from normal [15].
• Data suggest that kappa opioid agonist-induced water diuresis involves inhibition of vasopressin (AVP) secretion; however, it is not clear whether this action involves kappa receptors in the neurohypophysis or receptors behind the blood-brain barrier (BBB) [14].
• In contrast, camostat mesilate is slowly absorbed (8%/hr) and could inhibit the proteolytic activity in the nasal mucosa, resulting in enhanced nasal absorption of AVP and 1-d-8-DAVP [18].

Associations of AVP with chemical compounds

• Plasma vasopressin (AVP) concentration in dogs anaesthetized with chloralose was measured by radioimmunoassay and was within the range of 2-5 pg/ml. during control periods [16].
• However, the ACTH and aldosterone responses to 5 ng/kg.min angiotensin II infusion iv were attenuated in neurohypox dogs off AVP replacement [17].
• However, AVP 10(-8) M increased the lumen diameter of norepinephrine (NE)-constricted afferent arterioles pretreated with OPC21268 (OPC + NE, 8.2 +/- 0.7 microns; OPC + NE + AVP, 9.9 +/- 0.9 microns*; *P < 0.05, N = 13) [8].
• AVP and IBMX changed the direction of net fluid transport to secretion (4.24 +/- 0.49 x 10(-6) ml/min/cm2) [12].
• This vasodilatory effect of AVP was abolished by pretreatment with a V2 antagonist, OPC31260 [8].

Other interactions of AVP

• The nature of the activity of vasopressin which is responsible for the inhibition of renin secretion was studied by comparing the effects of vasopressin (AVP) and analogs of AVP in anesthetized water-loaded dogs [19].

Analytical, diagnostic and therapeutic context of AVP

• Three weeks after transplantation the AVP measurements were consistent with an insufficient venous system, whereas the VRT90 measurements were between and statistically different from both the control and totally incompetent system (p less than 0.05) [15].
• TWI per kg body weight ( TWI X kg-1) after 90 min was significantly correlated with the osmolalities and AVP levels in plasma and CSF prior to rehydration [20].
• Simultaneous intravenous infusion of AVP (12.5 ng/min) had a small, augmenting effect on the ACTH response to NP (peak ACTH 120 +/- 27 pg/ml) [21].
• After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)[22]
• Adrenalectomy attenuated AVP response to hemorrhagic hypotension [10].

References