Conivaptan, a Selective Arginine Vasopressin V1a and V2 Receptor Antagonist Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest via Perivascular Pool of Aquaporin-4

2016 ◽  
Vol 24 (2) ◽  
pp. 273-282 ◽  
Author(s):  
Shin Nakayama ◽  
Mahmood Amiry-Moghaddam ◽  
Ole Petter Ottersen ◽  
Anish Bhardwaj
Keyword(s):  
Cardiac Arrest ◽  
Receptor Antagonist ◽  
Cerebral Edema ◽  
Arginine Vasopressin ◽  
Aquaporin 4 ◽  
V2 Receptor ◽  
V2 Receptor Antagonist

Arginine vasopressin produces renal vasodilation via V2 receptors in conscious dogs

1993 ◽  
Vol 265 (4) ◽  
pp. R934-R942 ◽  
Author(s):  
M. Naitoh ◽  
H. Suzuki ◽  
M. Murakami ◽  
A. Matsumoto ◽  
A. Ichihara ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Receptor Antagonist ◽  
Arginine Vasopressin ◽  
Statistical Significance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Vasodilatory Response ◽  
V2 Receptor ◽  
Plasma Arginine ◽  
V2 Receptor Antagonist

In conscious dogs, 36-h water deprivation induced a significant increase in renal blood flow (RBF) with elevation of the plasma arginine vasopressin (AVP) concentration to 9.6 +/- 1.8 pg/ml. To simulate such a condition, a mild elevation of plasma AVP was produced by infusing AVP intravenously at a dose of 0.1 ng.kg-1.min-1 for 20 min. The plasma AVP concentration then increased to 6.8 +/- 0.7 pg/ml. This dose of AVP increased the RBF by 21.7 +/- 2.6% and decreased the renal vascular resistance by 18.1 +/- 2.3% without significant changes in mean arterial pressure, cardiac output, or heart rate. The mechanism of this renal vasodilatory action was examined using newly developed, orally effective, selective AVP antagonists OPC-21268 (a V1-receptor antagonist) and OPC-31260 (a V2-receptor antagonist). In 36-h water-deprived dogs, V2-receptor blockade with OPC-31260 significantly decreased the RBF by 20.5 +/- 2.6% without significant changes in cardiac output. The exogenous AVP-induced renal vasodilatory response tended to be augmented when V1 receptors were blocked by pretreatment with OPC-21268, but the change did not achieve statistical significance. On the other hand, V2-receptor blockade by either pretreatment with OPC-31260 or simultaneous infusion of OPC-31260 inhibited this vasodilatory response. Furthermore, intravenous infusion of 1-desamino-8-D-arginine vasopressin (DDAVP) at a dose of 0.3 ng.kg-1 x min-1 for 20 min significantly increased the RBF by 36.5 +/- 1.7%, and this DDAVP-induced renal vasodilation was inhibited by simultaneous infusion of V2-receptor antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular Responses to Vasopressin Antagonists in Man and Rat

1994 ◽  
Vol 87 (4) ◽  
pp. 389-395 ◽  
Author(s):  
Louise M. Burrell ◽  
Paddy A. Phillips ◽  
K. A. Rolls ◽  
B. F. Buxton ◽  
C. I. Johnston ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Arginine Vasopressin ◽  
Resistance Arteries ◽  
Antagonist Activity ◽  
Receptor System ◽  
Mammary Arteries ◽  
Internal Mammary ◽  
V2 Receptor ◽  
V2 Receptor Antagonist

1. The effects of the non-peptide arginine vasopressin V1 receptor antagonist (OPC-21268) and the non-peptide V2 receptor antagonist (OPC-31260) on vasopressin-induced contraction of human internal mammary arteries and rat mesenteric resistance arteries were investigated. 2. In human internal mammary arteries, the non-peptide V1 receptor antagonist, OPC-21268, failed to antagonize vasopressin-induced contraction at low concentrations and potentiated the contraction at higher concentrations (300 nmol/l, P < 0.05). A peptide selective V1 receptor antagonist {[d(CH2)5, sarcosine7]arginine vasopressin} potently inhibited the vasopressin-induced contraction, indicating the presence of functionally constrictor V1 receptors in human internal mammary arteries. Both peptide (desGly-NH29[d(CH2)5, D-Ile2, Ile4]arginine vasopressin) and non-peptide ‘selective’ V2 receptor antagonists (OPC-31260, 3 μmol/l) significantly antagonized vasopressin-induced contraction (P < 0.01), indicating partial V1 receptor antagonist activity. 3. The vasopressin-induced contraction in human internal mammary arteries was reversed by high concentrations of the non-peptide V2 receptor antagonist, OPC-31260, but not by the non-peptide V1 receptor antagonist, OPC-21268. 5. In rat mesenteric resistance arteries, both OPC-21268 (10 nmol/l) and OPC-31260 (1 μmol/l) antagonized vasopressin-induced contraction (P < 0.01). 6. The results of this study in vitro indicate that in human internal mammary arteries, the non-peptide OPC-21268 is a partial V1 receptor agonist with no V1 receptor antagonist activity, whereas the non-peptide OPC-31260 acts as a V1 receptor antagonist. Both OPC-21268 and OPC-31260 have V1 receptor antagonistic activity in vitro in the rat mesenteric resistance arteries. 7. These findings illustrate the complexity of the vasopressin receptor system and highlight the variability in results with peptide or non-peptide vasopressin analogues, between studies in vivo or in vitro, between species and across vascular beds.

scholarly journals A new selective, and sensitive method for the determination of lixivaptan, a vasopressin 2 (V2)-receptor antagonist, in mouse plasma and its application in a pharmacokinetic study

2018 ◽  
Vol 16 (1) ◽  
pp. 614-620
Author(s):  
Haitham Alrabiah ◽  
Mohammed Abunassif ◽  
Sabry Attia ◽  
Gamal Abdel-Hafiz Mostafa
Keyword(s):  
Receptor Antagonist ◽  
Pharmacokinetic Study ◽  
Limit Of Detection ◽  
Internal Standard ◽  
Hplc Method ◽  
Maximum Plasma ◽  
Mouse Plasma ◽  
V2 Receptor ◽  
V2 Receptor Antagonist

AbstractA new, selective and sensitive HPLC method for the determination of lixivaptan, an oral selective vasopressin 2 (V2)-receptor antagonist, was investigated and validated. A Waters symmetry C18 column was used as a stationary phase in isocratic elution mode using a mobile phase composed of KH2PO4 (100 mM)-acetonitrile (40: 60, v/v) at a flow rate of 1.5 mL min-1. Diclofenac was used as the internal standard (IS). Lixivaptan and the IS were extracted from plasma by protein precipitation and were detected at 260 nm. Lixivaptan and diclofenac were eluted at 3.6 and 6.2 min, respectively. The developed method showed good linearity over the calibration range of 50 -1000 ng mL-1 with a lower limit of detection of 16.5 ng mL-1. The extraction percentage of lixivaptan in the mouse plasma was in the range of 88.88 - 114.43%, which indicates acceptable extraction. The aforementioned method was validated according to guidelines of the International Council on Harmonization (ICH). The intra- and inter-day coefficients of variation did not exceed 5.5%. This method was presented to be simple, sensitive, and accurate and was successfully adapted in a pharmacokinetic study of the profile of lixivaptan in mouse plasma. A mean maximum plasma concentration of lixivaptan of 113.82 ng mL-1 was achieved in 0.5 h after oral administration of a 10 mg kg-1 dose in mouse as determined using the developed method.

Inhibition of renal cystic disease development and progression by a vasopressin V2 receptor antagonist

10.1038/nm935 ◽  
2003 ◽  
Vol 9 (10) ◽  
pp. 1323-1326 ◽  
Author(s):  
Vincent H Gattone ◽  
Xiaofang Wang ◽  
Peter C Harris ◽  
Vicente E Torres
Keyword(s):  
Receptor Antagonist ◽  
Disease Development ◽  
Cystic Disease ◽  
Renal Cystic Disease ◽  
Vasopressin V2 Receptor ◽  
V2 Receptor ◽  
Vasopressin V2 Receptor Antagonist ◽  
V2 Receptor Antagonist

Effect of SR121463, a Selective Non-Peptide Vasopressin V2 Receptor Antagonist, in a Rabbit Model of Ocular Hypertension

2000 ◽  
Vol 16 (3) ◽  
pp. 203-216 ◽  
Author(s):  
FREDERIC LACHERETZ ◽  
ALAIN BARBIER ◽  
CLAUDINE SERRADEIL-LE GAL ◽  
PIERRE-PAUL ELENA ◽  
JEAN-PIERRE MAFFRAND ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Ocular Hypertension ◽  
Rabbit Model ◽  
Vasopressin V2 Receptor ◽  
V2 Receptor ◽  
Vasopressin V2 Receptor Antagonist ◽  
V2 Receptor Antagonist
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