Disease relevance of AVP

• Five heart groups (cold) were perfused with AVP, D-ARG, L-ARG, L-NAME, or nothing (control), but after 2 hours they were perfused at low flow for 22 hours at 3.7 degrees C and again for 3 hours at 37.5 degrees C. ADE, butanedione monoxime, and NP were given for cardioprotection before, during, and after hypothermia [1].
• BACKGROUND: The purpose of the study was to compare initial resuscitation with arginine vasopressin (AVP), phenylephrine (PE), or isotonic crystalloid fluid alone after traumatic brain injury and vasodilatory shock [2].
• From these data we assume a simultaneous activation of peripheral and central release of AVP with antidiuretic and antipyretic effects by dehydration [3].
• Measurements were performed at baseline, after E. coli lipopolysaccharide (LPS) administration and at 20 min intervals during incremental AVP infusion (n=8; 0.014, 0.029, 0.057, 0.114 and 0.229 IU kg(-1) h(-1), respectively) or infusion of saline (n =8) [4].
• In this report, we present electrophysiological evidence that arginine-vasopressin (AVP) is a neurotransmitter in guinea pig inferior mesenteric ganglion (IMG) [5].

Psychiatry related information on AVP

• In dehydrated animals (24 h water deprivation) the arterial blood plasma level of AVP doubled causing antidiuretic effects [3].
• Lithium, a drug frequently used for treatment of affective disorders, is known to cause a vasopressin-resistant state, leading to polyuria and polydipsia [6].

High impact information on AVP

• Plasminogen activator (PA) production in LLC-PK1 pig kidney cell culture is induced to high levels by calcitonin and vasopressin, both of which stimulate adenylate cyclase, or by other compounds that also raise intracellular cAMP levels [7].
• The hypothalamo-neurohypophyseal complex (HNC) of the fetal guinea pig shows a dramatic increase in its content of vasopressin and neurophysin between the 40th and 55th days of gestation [8].
• Vasopressin and epinephrine for cardiac arrest [9].
• Without shock, central intravenous infusions of angiotensin II (but not norepinephrine or vasopressin) closely mimicked this selective vasoconstriction [10].
• Prior blockade of the renin-angiotensin axis ablated this response and eliminated the mesenteric contribution to systemic vascular resistance, while confirmed blockade of the alpha-adrenergic system or vasopressin system had no effect [10].

Chemical compound and disease context of AVP

• With developing congestive heart failure (CHF), activation of the vasopressin V(1a) and angiotensin II type 1 (AT(1)) receptors can occur [11].
• INTERVENTIONS: After 4 mins of ventricular fibrillation and 3 mins of basic life support, the pigs were randomly assigned to receive either 200 microg/kg epinephrine, 0.4 units/kg vasopressin alone, or 45 microg/kg norepinephrine plus 45 microg/kg epinephrine plus 0.4 units/kg vasopressin before defibrillation [12].
• Heterogeneity of the vasoconstrictor effect of vasopressin in septic shock [13].
• These data suggest that vasopressin modulates NOC/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury in an age-dependent manner [14].
• OBJECTIVE: To investigate whether the vasopressin analog terlipressin might induce hepatosplanchnic ischemia during long-term, hyperdynamic, volume-resuscitated porcine endotoxemia [15].

Biological context of AVP

• Left ventricular pressure and cardiac efficiency improved more in the postcold L-ARG group than in the postcold D-ARG, AVP, and L-NAME groups [1].
• In addition, when AVP and inulin were injected into the amniotic sac in vivo during the last week of gestation, the AVP to inulin ratio decreased (P less than 0.05) over a 2-h period, indicating a swallowing-independent disappearance of AVP [16].
• Moreover, slow excitatory postsynaptic potentials (EPSPs) elicited by repetitive nerve stimulation were attenuated in 75% of cells tested in the presence of excess AVP, and occasionally in the presence of the antagonist [5].
• Coronary vasoconstriction was elicited by perfusing hearts with increasing concentrations of AVP in random order [17].
• We found that AVP increased coronary vascular resistance more at CCF than at CPP [17].

Anatomical context of AVP

• In our experimental conditions, in which myocytes were bathed in Ca(2+)-free high-potassium solutions, AVP-induced potentiation was observed without changes in [Ca2+]i measured by fura 2 fluorescence signals (estimated [Ca2+]i, approximately 80 nmol/L) [18].
• A maximally active concentration of AVP (1 microM) increased adenylate cyclase activity in canine renal plasma membranes to a value 2.7 times that of basal activity [19].
• Histidine and imidazole but not alanine (the histidine core structure) increase basal, GTP-, forskolin-, and AVP-stimulated adenylate cyclase activity in LLC-PK1 membranes [20].
• We explored whether overexpression of one of the cAMP-PDE type isozymes, PDE-IV, in [8-Arg]-vasopressin (AVP) sensitive renal epithelial LLC-PK1 cells can prevent the hormone-elicited cAMP increase [21].
• Tritiated AVP incubated in only amniotic fluid produced M2, with only slight M1 production [16].

Associations of AVP with chemical compounds

• However, AVP stimulates adenylate cyclase activity in a dose-dependent fashion with an EC50 of 14 nM, whereas OT or dVDAVP has no effect at 100 nM [22].
• These pharmacological properties are distinct from the previously described V1 and V2 vasopressin receptors and indicate the presence of a new class of AVP receptors [22].
• Lysine vasopressin and the V1 antagonist [1-deaminopenicillamine, 2-(O-methyl)tyrosine]Arg8-vasopressin compete with high affinity with [3H]AVP binding, whereas the V2 agonist [1-deamino,4-valine]D-Arg8-vasopressin (dVDAVP) is 110 times less potent than AVP [22].
• In warm groups, L-ARG did not alter basal flow or ADE, ACh, 5-HT, or NP responses, whereas L-NAME and AVP reduced basal flow and the ADE response, abolished ACh and 5-HT responses, and increased the NP response [1].
• The explants in the group treated with 7.4 X 10(-5) M indomethacin for 60 min before the experiment and throughout the experiment responded to 6.5 X 10(-8) M angiotensin II with a 166 +/- 42% increase in AVP release over control release [23].

Regulatory relationships of AVP

• It is concluded that AVP directly inhibits secretin-stimulated ductal fluid secretion in the guinea pig pancreas [24].
• The aquaporins (AQPs) are a family of homologous water-channel proteins that can be inserted into epithelial cell plasma membranes either constitutively (AQP1) or by regulated exocytosis following vasopressin stimulation (AQP2) [25].
• Vasopressin (100 mU/ml) failed to induce a translocation of PKC alpha from the C to the PM [26].
• Central and peripheral doses of cholecystokinin that inhibit feeding in pigs also stimulate vasopressin and cortisol release [27].

Other interactions of AVP

• Similar tests on alpha-methyl-D-glucoside uptake showed that serum, TPA, PTH, and AVP had no significant effect on phlorizin-sensitive uptake; however, calcitonin increased uptake by 84% (n = 18) [28].
• Previously, we have shown in porcine inner medullary collecting duct (IMCD) cells that endothelin (ET), probably in an autocrine fashion, suppresses arginine vasopressin (AVP)-induced synthesis of cAMP and thereby, may modify the action of AVP on IMCD fluid transport [29].
• Activation of protein kinase C (PKC) with phorbol esters inhibited PTH and AVP responses and 8-BrcAMP-induced [Ca2+]i transients.(ABSTRACT TRUNCATED AT 250 WORDS)[30]
• We examined the effects of [Arg8]-vasopressin (AVP) on long term potentiation (LTP) of the field excitatory postsynaptic potentials at CA1 and CA3 synapses in adult guinea pig hippocampal slices [31].
• In the isolated vascularly perfused pancreas, AVP reduced secretin-stimulated fluid secretion and increased the vascular resistance when the perfusion rate was held constant [24].

Analytical, diagnostic and therapeutic context of AVP

• The effect of prostaglandins (PGs) on arginine vasopressin (AVP) release was investigated using the male guinea pig hypothalamo-neurohypophyseal complex (HNC) in organ culture [23].
• When fetal plasma, urine, and amniotic fluid were fractionated on HPLC, AVP was identified only in fetal plasma and urine [16].
• Effluent fractions were monitored for corticotrophin-releasing factor (CRF) bioactivity, using the perfused isolated pituitary cell column bioassay, and radioimmunoassay for CRF-41, AVP, oxytocin, neurophysin, adrenocorticotrophic hormone (ACTH) and luteinizing hormone-releasing hormone (LHRH) [32].
• In the presence of tetrodotoxin, OFQ/N hyperpolarized 48 of 48 SON magnocellular neurons, 24 of which were subsequently identified by immunocytochemistry as arginine vasopressin positive (AVP+) [33].
• Production of cAMP could be detected in BIB27 cells even 12 h after treatment with AVP or SCT, whereas cAMP production in LLC-PK1 had returned to basal within 1 and 8 h, respectively [34].

References