Human Reproduction, Vol. 15, No. 12, 2496-2503,
December 2000
© 2000 European Society of Human Reproduction and Embryology
Oestrous cycle and pregnancy alter the reactivity of the rat uterine vasculature
1 Center for Applied Microcirculatory Research and 2 Department of Physiology, Health Sciences Center, A1115, University of Louisville School of Medicine, Louisville, KY 40292, USA
Isolated uterine vascular beds from virgin and pregnant rats were used to assess vascular reactivity and the ability of nitric oxide (NO), prostanoids and endothelium-derived hyperpolarizing factor (EDHF) to modulate these responses. One uterine horn from female rats in each oestrous cycle day and gestation day 17 was removed and perfused with physiological saline solution. Tone was induced with cirazoline (1 µmol/l), and concentration–response curves to acetylcholine (ACh) generated. Responsiveness to ACh was tested in the presence of N-nitro-L-arginine (L-NA), ibuprofen (IBU) and tetrabutylammonium (TBA), to inhibit NO synthase, cyclo-oxygenase and K+ channels respectively. Cirazoline-induced tone was smaller in the pregnant compared with the proestrous group. Sensitivity to ACh was cycle day and pregnancy dependent with pregnant > dioestrous day-1 > dioestrous day-2 > proestrous and oestrous. L-NA shifted the curve to the right in all groups except dioestrous day-1. IBU inhibited the ACh response in the pregnant group only. TBA virtually abolished the response in all groups. These results suggest that in the uterine vascular bed from pregnant rats, EDHF, along with NO and a dilator prostanoid mediate ACh-induced dilatation. In contrast, in the dioestrous day-1 group, only EDHF seems to be released by ACh in this vascular bed. In the oestrous, dioestrous day-2 and proestrous groups, ACh releases both EDHF and NO.
Key words: acetylcholine/oestrous cycle/pregnancy/uterus/vascular reactivity
3 To whom correspondence should be addressed. E-mail: nlalsi01{at}gwise.louisville.edu
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  N. I. Gokina and T. Goecks Upregulation of endothelial cell Ca2+ signaling contributes to pregnancy-enhanced vasodilation of rat uteroplacental arteries Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H2124 - H2135. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. St-Louis, B. Sicotte, A. Beausejour, and M. Brochu Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake Reproduction, February 1, 2006; 131(2): 331 - 339. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Benoussaidh, Y. Maurin, and O. Rampin Possible neural mediation of the central effects of oxytocin on uterine motility Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2005; 289(3): R798 - R804. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Mateev, A. H. Sillau, R. Mouser, R. E. McCullough, M. M. White, D. A. Young, and L. G. Moore Chronic hypoxia opposes pregnancy-induced increase in uterine artery vasodilator response to flow Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H820 - H829. [Abstract] [Full Text] [PDF]
|
|