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Placental Insufficiency Leads to Developmental Hypertension and Mesenteric Artery Dysfunction in Two Generations of Sprague-Dawley Rat Offspring¹

College of Nursing³ and Department of Pharmacology, Physiology and Therapeutics,⁴ University of North Dakota, Grand Forks, North Dakota, 58202

ABSTRACT

It is generally accepted that preeclampsia results from reduction in perfusion to the uteroplacental unit leading to maternal hypertension and fetal growth restriction. Placental insufficiency creates an environment of fetal undernutriton, predisposing the fetus to the development of adult disease. In this study, we characterized the development and perpetuation of hypertension in two generations of male and female offspring subjected to an environment of fetal undernutrition via reduced uteroplacental perfusion pressure. Further, we examined vascular responses of resistance arteries in these animals to determine the influence of placental insufficiency on the development and perpetuation of hypertension. Experimental dams underwent a surgical procedure to reduce uteroplacental perfusion pressure, with resulting offspring comprising the first generation (F1). One male and one female from each of the F1 experimental litters served as breeders of the second generation (F2). Weekly systolic blood pressure measurements were obtained from 4 to 24 wk in control, F1, and F2 offspring. Vascular responsiveness to the vasoconstrictors phenylephrine and potassium chloride and the vasorelaxants acetylcholine and sodium nitroprusside was determined in the three offspring groups at 6, 9, and 12 wk of age. Our findings indicate that placental insufficiency during a critical developmental window in late gestation leads to hypertension in juvenile Sprague-Dawley rat offspring and is perpetuated in a second generation of offspring in a gender-specific manner. Further, exposure to placental insufficiency during late gestation leads to developmental alterations characterized by vascular hyperresponsiveness, perpetuated to a second generation of offspring in the absence of persistent environmental stimuli, contributing to hypertension.

developmental biology

² Correspondence: Cindy M. Anderson, Box 9025, College of Nursing, University of North Dakota, Grand Forks, ND 58202-9025. FAX: 701 777 4096; cindyanderson{at}mail.und.nodak.edu

¹ Supported by the University of North Dakota Faculty Seed Money Council; Sigma Theta Tau International, Eta Upsilon Chapter; University of North Dakota College of Nursing (C.M.A.); and National Institute of Digestive, Diabetes and Kidney Disease (J.N.B.) DK51430.