Prenatal stress in the rat results in increased blood pressure responsiveness to stress and enhanced arterial reactivity to neuropeptide Y in adulthood.

We have shown previously that stress in the pregnant rat leads to a heightened cardiovascular response to restraint in adult offspring. The present study was undertaken to explore further the persistent cardiovascular effects of prenatal stress, with a focus on peripheral vascular function. Sprague-Dawley female rats were exposed to restraint/bright light three times daily in the last week of pregnancy. Litters from stressed and control females were cross-fostered to control dams to eliminate possible effects of maternal stress on nursing behaviour. At 120 days, offspring cardiovascular variables were measured by radiotelemetry. Reactivity of mesenteric small arteries was assessed by myography, and responses to electrical field stimulation determined. Resting cardiovascular parameters in prenatally stressed (PS) offspring were similar to controls but PS rats showed a greater increase in systolic blood pressure following restraint stress (P<0.05). Recovery was also prolonged in PS animals compared with controls and was of longer duration in PS females than in PS males (P<0.05). Adult PS females, but not males, also had elevated basal plasma corticosterone levels in comparison with controls (P<0.05). Vascular reactivity to neuropeptide Y (P<0.05) and electrical field stimulation (P<0.05) in mesenteric arteries was also significantly increased in PS animals. Vascular responses to adrenergic agonists as well as endothelial dilator function did not differ between PS and controls. We conclude that prenatal stress during late gestation has long-lasting effects on cardiovascular responsiveness and vascular reactivity to neuropeptide Y in the offspring.