(d(CH2)51,Tyr(Me)2,Arg8)-Vasopressin

Dissociation of the anxiolytic-like effects of Avpr1a and Avpr1b receptor antagonists in the dorsal and ventral hippocampus.[Pubmed:18508119]

Neuropeptides. 2008 Aug;42(4):411-21.

Arginine-vasopressin (AVP) is synthesized and released centrally in several brain structures. AVP is thought to mediate anxiety-related behavior through two central receptor subtypes, Avpr1a and Avpr1b. Although these AVP receptor subtypes are expressed in several brain regions, including the hippocampus, little is known about their explicit role in unconditioned fear or anxiety. This experiment assessed the anxiety-related effects of a selective Avpr1a antagonist ([beta-Mercapto-beta,beta-cyclopentamethylenepropionyl1, O-me-Tyr2, Arg8]-AVP) and a selective Avpr1b antagonist ((2S,4R)-1-[5-chloro-1-[(2,4-dimethoxyphenyl)sulfonyl]-3-(2-methoxy-phenyl)-2-oxo -2,3-dihydro-1H-indol-3-yl]-4-hydroxy-N,N-dimethyl-2-pyrrolidine carboxamide; SSR 149415) microinfused into either the dorsal or ventral sub-regions of the rat hippocampus. Avpr1a antagonism in the ventral, but not the dorsal hippocampus reduced rats' anxiety-like behavior in the elevated plus-maze test. Conversely, Avpr1b antagonism in the dorsal, but not the ventral, hippocampus reduced anxiety in the plus-maze test. Neither antagonist reduced anxiety-like behavior in the shock-probe burying test. Overall, the results show that both receptor subtypes of AVP are involved in anxiety-related responses, but their specific contributions depend on three variables: (1) the anxiety-related response (shock-probe avoidance versus open-arm avoidance), (2) the receptor subtype antagonized (Avpr1a versus Avpr1b), and (3) the area of hippocampus (dorsal versus ventral) into which these antagonists are infused. These dissociations suggest that different fear responses are under the control of specific AVP receptor systems within discrete parts of the hippocampus.

Vasopressin inhibits sarcolemmal ATP-sensitive K+ channels via V1 receptors activation in the guinea pig heart.[Pubmed:11922278]

Circ J. 2002 Mar;66(3):277-82.

To examine the effect of vasopressin on the sarcolemmal ATP-sensitive K (K(ATP)) channel, cell-attached, insideout and open-cell-attached methods of patch clamp techniques were used in isolated guinea pig ventricular myocytes. Suppressing both glycolytic and oxidative ATP production attained K(ATP) channel activation. In the cell-attached mode, vasopressin inhibited KATP channels in a concentration-dependent manner with an IC50 of 15.1+/-1.8 nmol/L. In the inside-out configuration, vasopressin failed to block K(ATP) channels. In the cell-attached mode, manning compound (1 micromol/L), a V1 receptor-selective antagonist, blocked the inhibitory action of vasopressin, although OPC-31260 (1 micromol/L), a V2 receptor-selective antagonist could not affect the action of vasopressin. In addition, vasopressin lost its inhibitory action on K(ATP) channels when the channel was activated by pinacidil, a K channel opener and in the open-cell-attached mode effected by streptolysin-O. Thus, the inhibitory action of vasopressin K(ATP) channels may occur via V1 receptor related mechanism.

Arginine vasopressin and oxytocin increase intracellular calcium and cAMP in human glomerular epithelial cells in culture.[Pubmed:8871886]

Kidney Blood Press Res. 1996;19(2):81-6.

The signal transduction linkages of arginine vasopressin (AVP) and oxytocin receptors were investigated in human glomerular epithelial cells (GEC) in culture. AVP (ED50, 10(-7) mol/l) and oxytocin (ED50, 3 x 10(-8) mol/l) induced a rapid, transient and dose-dependent increase in [Ca2+]i as detected by fura-2 microfluorimetry. The baseline of [Ca2+]i in human GEC was 109 +/- 2.8 nmol/l (n = 60). The V1a receptor antagonist [d(CH2)5(1), Tyr(Me)2, Arg8]-vasopressin inhibited the AVP-(IC50, 5 x 10(-9) mol/l) and oxytocin-induced (IC50, 3 x 10(-8) mol/l) increase in [Ca2+]i in a dose-dependent manner. Both, AVP and oxytocin caused accumulation of cAMP. The AVP-stimulated cAMP increase was blocked by pretreatment of human GEC with the V1a receptor antagonist (10(-7) mol/l), whereas the oxytocin-induced cAMP accumulation remained uninfluenced. In conclusion the present results indicate that: (1) V1a receptor activation, AVP and oxytocin induce a transient elevation in [Ca2+]i in human GEC; (2) AVP and oxytocin cause cAMP accumulation; (3) the AVP-induced cAMP accumulation is inhibited by a V1a receptor antagonist, whereas (4) the oxytocin response showed no effect. In addition, a different receptor might be possible, at least in oxytocin-induced-cAMP accumulation.