Relaxation of human isolated mesenteric arteries by vasopressin and desmopressin

Abstract

1 The effects of vasopressin and deamino-8-D-arginine vasopressin (DDAVP, desmopressin) were studied in artery rings (0.8-1 mm in external diameter) obtained from portions of human omentum during the course of abdominal operations (27 patients). 2 In arterial rings under resting tension, vasopressin produced concentration-dependent, endotheliumindependent contractions with an EC% of 0.59 ± 0.12 nM. The V, antagonist d(CH2)5Tyr(Me)AVP (1 f1M) and the mixed V1-V2 antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (0.01 JAM) displaced the control curve to vasopressin to the right in a parallel manner without differences in the maximal responses. In the presence of indomethacin (1 AM) the contractile response to vasopressin was significantly increased (P <0.01). 4 The selective V2 receptor agonist, DDAVP, caused endothelium-independent, concentration-dependent relaxations in precontracted arterial rings that were inhibited by the mixed V1-V2 receptor antagonist, but not by the VI receptor antagonist or by pretreatment with indomethacin or L-NAME.5 Results from this study suggest that vasopressin is primarily a constrictor of human mesenteric arteries by VI receptor stimulation; vasopressin causes dilatation only during VI receptor blockade. The relaxation appears to be mediated by the release of vasodilator prostaglandins from the endothelial cell layer and is independent of V2 receptor stimulation or release of nitric oxide. In contrast, the relaxation induced by DDAVP is largely dependent on stimulation of V2 receptors.

Arginine Vasopressin in Advanced Vasodilatory Shock

“…In low dosages, AVP-mediated vasodilatation of the splanchnic vascular bed has been reported. 31 Significantly improved systemic perfusion pressure may further explain lower PrCO 2 and Pr-aCO 2 in patients receiving AVP. However, it must be considered that gastric tonometry does not directly measure gastrointestinal perfusion and cannot be regarded as an accurate indicator of splanchnic circulation under pathophysiological conditions.…”

Arginine Vasopressin Enhances Sympathetic Constriction Through the V 1 Vasopressin Receptor in Human Saphenous Vein

“…[22][23][24] In view of the specificity and potency of the V 1 antagonist d(CH 2 ) 5 Tyr(Me)AVP, it seems appropriate to consider the use of V 1 receptor antagonists in circumstances in which AVP plasma concentrations are raised. Furthermore, provided that V 1 receptor blockade is present, AVP induces marked dilatation of previously contracted human arteries 5 and saphenous veins, 21 probably because of the release of vasodilatory prostaglandins from the vessel wall. These findings could explain the reduction of vascular resistance that has been observed after intravenous administration of the V 1 antagonist d(CH 2 ) 5 Tyr(Me)AVP in patients with hypertension or congestive heart failure in the presence of high plasma AVP levels.…”

“…This effect is endothelium independent and due to direct stimulation of receptors located on smooth muscle cells. 5,9,10 Further studies of the physiological effects of AVP have implicated a possible role of V 2 receptors in mediating vasodilation in some vascular beds. [11][12][13][14] AVP may also modify the effects of other vasoactive substances that are found in plasma or released from perivascular nerve endings.…”

Contractile responses of human thyroid arteries to vasopressin

“…With regard to human vessels, vasopressin causes powerful V 1 receptor-mediated constriction in isolated mesenteric (Ohlstein and Berkowitz, 1986;Martínez et al, 1994b), cerebral (Lluch and Gómez, 1987;White and Robertson, 1987) and renal (Medina et al, 1996b) arteries. This effect is endothelium-independent and due to direct stimulation of receptors located on smooth muscle cells (Martín de Aguilera et al, 1990;Martínez et al, 1994a, b).…”