Arginine vasopressin, via activation of post-junctional V1 receptors, induces contractile effects in mouse distal colon

Abstract

The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator of intestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVP on the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism. Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP (0.001 nM-100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle, antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin, atropine and indomethacin. Contractile response to AVP was reduced in Ca 2+ -free solution or in the presence of nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. U-73122, an inhibitor of the phospholipase C, effectively antagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatory effect in the longitudinal muscle of distal colon at very high concentrations, effect antagonized by V-1880. The results of this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity of longitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis. Contractile response is achieved by increase in cytoplasmatic Ca 2+ concentration via extracellular Ca 2+ influx from L-type Ca 2+ channels and via Ca 2+ release from intracellular stores through phospholipase C pathway.No modulation has been observed on the contractility of the circular muscle.

Angiotensin II type II receptors and colonic dysmotility in 2,4‐dinitrofluorobenzenesulfonic acid‐induced colitis in rats

“…In control animals, the contractile effect of Ang II was dependent on AT 1 receptor activation, as pretreatment with Losartan, AT 1 receptor antagonist, significantly antagonized Ang II effect, and PD123319, AT 2 receptor antagonist was ineffective. This is line with previous studies addressing AT 1 receptors as the major effectors of Ang II‐related effects and AT 2 receptors, even if expressed, seems uncoupled to the contractile mechanisms in physiological conditions . In DNBS‐treated animals, the contractile effect of Ang II was still antagonized by the AT 1 receptor antagonist, indicating that Ang II‐induced contractile effect is once more mediated by AT 1 receptors.…”

“…Each preparation was tested with a single antagonist, unless otherwise stated. Concentrations of the drugs used were determined from previous experiments and from literature.…”

Vasopressin-induced mouse urethral contraction is modulated by caveolin-1

“…V 1a and V 1b receptors couple to Gq whereas V 2 receptors couple to the Gs pathway (Koshimizu et al, 2012). The V 1a receptor is expressed by smooth muscle cells where its activation causes vasoconstriction, increased intestinal motility and bladder contraction (Holmquist et al, 1991;Mastropaolo et al, 2013;Thibonnier et al, 1999;Uvelius et al, 1990). The V 2 receptor, on the other hand, is responsible for the antidiuretic action of AVP via effects on the collecting ducts of the kidneys (Thibonnier et al, 1999;Treschan and Peters, 2006).…”

Vasopressin regulation of epithelial colonic proliferation and permeability is mediated by pericryptal platelet‐derived growth factor A

“…; Mastropaolo et al . ). Preliminary studies showed that the effects of AVP were concentration dependent and that the responses were maximal using 10 n m AVP.…”