HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Anderson, C. M. Articles by Benoit, J. N. Search for Related Content PubMed PubMed Citation Articles by Anderson, C. M. Articles by Benoit, J. N.

---

ORIGINAL RESEARCH ARTICLE

Mesenteric Vascular Responsiveness in a Rat Model of Pregnancy-Induced Hypertension

Cindy M. Anderson^*,,1, Faye Lopez, Hai-Ying Zhang, Yuichi Shirasawa, Kristin Pavlish and Joseph N. Benoit

^* College of Nursing and Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota, Grand Forks, North Dakota 58202

To whom requests for reprints should be addressed at ¹ Box 9025, University Station, College of Nursing, 5th and Harvard Street, University of North Dakota, Grand Forks, ND 58202. E-mail: cindyanderson{at}mail.und.edu

Reduced perfusion to the placenta in early pregnancy is believed to be the initiating factor in the development of preeclampsia, triggering local ischemia and systemic vascular hyperresponsiveness. This sequence of events creates a predisposition to the development of altered vascular function and hypertension. This study was designed to determine the influence of placental insufficiency on the responsiveness of mesenteric resistance arteries in an animal model of preeclampsia. Placental insufficiency was induced by reduction in uteroplacental perfusion pressure (RUPP) in experimental Sprague-Dawley rat dams. The uterine branches of the ovarian arteries and the abdominal aortae of pregnant rats were surgically constricted on gestational Day 14. Dams in the control group underwent a sham procedure. Rats were euthanized on gestational Day 20, followed by removal of the small intestine and adjacent mesentery. First-order mesenteric resistance arteries were mounted on a small vessel wire myograph and challenged with incremental concentrations of vasoconstrictors and vasorelaxants. Mesenteric arteries in dams with placental insufficiency demonstrated an increased maximal tension to phenylephrine (7.15 ± 0.15 vs. 5.4 ± 0.27 mN/mm, P < 0.001); potassium chloride at 60 mM (3.43 ± 0.11 vs. 2.77 ± 0.14 mN/mm, P < 0.01) and 120 mM (3.92 ± 0.18 vs. 2.97 ± 0.16 mN/mm, P < 0.01); and angiotensin II (2.59 ± 0.42 vs. 1.51 ± 0.22 mN/mm, P < 0.05). Maximal relaxation to endothelium-dependent relaxants acetylcholine and calcium ionophore (A23187) was not significantly reduced. Data suggest that placental insufficiency leads to hyperresponsiveness to vasoconstrictor stimuli in mesenteric arteries.

Key Words: vascular smooth muscle • mesenteric artery • pregnancy-induced hypertension • placental insufficiency

This article has been cited by other articles:

				W. Chen and R. A. Khalil Differential [Ca2+]i signaling of vasoconstriction in mesenteric microvessels of normal and reduced uterine perfusion pregnant rats Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1962 - R1972. [Abstract] [Full Text] [PDF]