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Increased Myogenic Responses in Uterine but not Mesenteric Arteries from Pregnant Offspring of Diet-Restricted Rat Dams¹

Department of Obstetrics and Gynecology,⁴ Perinatal Research Centre, University of Alberta, Edmonton, Alberta Canada, T6G 2S2 Maternal and Fetal Health Research Centre,⁵ University of Manchester, St. Mary's Hospital, Whitworth Park, Manchester M13 0JH, United Kingdom

Results of epidemiological and animal studies suggest a link between poor in utero growth and cardiovascular disease in adult offspring. Few studies, however, have examined the effects of maternal undernutrition on the vasculature of pregnant female offspring, and to our knowledge, no studies have examined myogenic responses, which are essential to vascular tone development, in these animal models. Thus, myogenic responses were assessed in radial uterine arteries of pregnant female offspring to determine if diet restriction during pregnancy could contribute to transgenerational effects. These results were compared to those in mesenteric arteries, which greatly contribute to peripheral vascular resistance. Myogenic responses in the presence and absence of inhibitors for nitric oxide synthase (NOS) and prostaglandin H synthase (PGHS) were measured in arteries isolated from pregnant, 3-mo-old female offspring of control-fed (C_off) and globally diet-restricted (DR_off) rat dams. Although no differences were found in pregnancy weight gain, litter size, or fetal weights, placental size was significantly reduced in DR_off compared to C_off. Enhanced myogenic reactivity was observed at the highest pressure tested (110 mm Hg) in uterine, but not in mesenteric, arteries from DR_off compared to C_off. Inhibition of NOS, but not of PGHS, significantly increased myogenic responses in uterine arteries at pressures greater than 80 mm Hg in C_off but, interestingly, not in DR_off compared to untreated uterine arteries. Thus, impaired uterine vascular function in diet-restricted pregnant rat dams, which leads to similar impairment in their pregnant offspring, may be a mechanism through which transgenerational effects of unhealthy pregnancies occur.

¹ Supported by Canadian Institute of Health Research (CIHR). D.G.H. is a postdoctoral fellow supported jointly by Heart and Stroke Foundation of Canada and CIHR. S.V. is funded by through a Wyeth-Ayerst Fellowship Award and University of Alberta Perinatal Research Centre. P.N.B. is supported by Tommys: The Baby Charity. S.T.D. is a Canada Research Chair in Women's Cardiovascular Health and a Senior Scholar of the Alberta Heritage Foundation for Medical Research.

² Correspondence: Sandra T. Davidge, Perinatal Research Centre, 220 Heritage Medical Research Centre, University of Alberta, Edmonton, AB T6G 2S2, Canada. FAX 780 492 1308; sandra.davidge{at}ualberta.ca

³ D.G.H. and S.V. contributed equally to this work

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