Prostaglandin- or endothelium-mediated vasodilation is notinvolved in the blunted responses of blood vessels to vasoconstrictors in pregnant rats

Enhanced Vascular Reactivity During Inhibition of Nitric Oxide Synthesis in Pregnant Rats

“…These results are consistent with the findings of other laboratories. [7][8][9]11,12,23 This normal pregnancy-induced drop in blood pressure could be explained by changes in the function of the kidneys, metabolic changes, and/or changes in vascular reactivity. On the other hand, chronic NO synthase blockade with L-NAME caused severe hypertension in pregnant rats.…”

“…7,13 If this is the case, one would expect that blocking the formation of NO during pregnancy would bring the vascular reactivity back to the level observed in virgin rats. However, our data show that the vascular reactivity to phenylephrine in pregnant rats treated with L-NAME is greater than that in virgin rats.…”

“…6 This normal pregnancyassociated decrease in peripheral resistance has been explained by several mechanisms, including an increase in the metabolic requirements of both maternal and fetoplacental tissues and/or a decrease in vascular reactivity. 7 Several explanations have been proposed for the decrease in vascular reactivity during normal pregnancy, such as decreased pressor response to vasoconstrictors, 8 -10 specific alterations within the vascular wall, 11 and an increase in nitric oxide (NO) synthesis.12,13 Also, Conrad and Vernier 14 have found that the plasma level, metabolic production, and urinary excretion of cGMP, a second messenger of NO and a cellular mediator of vascular smooth muscle relaxation, are increased during pregnancy.In 5% to 7% of pregnancies, women develop a condition called pregnancy-induced hypertension.15 In contrast to normal pregnancy, pregnancy-induced hypertension is characterized by increased arterial blood pressure, generalized vasoconstriction, increased systemic vascular resistance, increased capillary permeability, decreased plasma volume, severe edema, increased intravascular coagulation, reduced tissue perfusion, decreased glomerular filtration rate, proteinuria, and widespread vascular endothelial damage. …”

“…6 This normal pregnancyassociated decrease in peripheral resistance has been explained by several mechanisms, including an increase in the metabolic requirements of both maternal and fetoplacental tissues and/or a decrease in vascular reactivity. 7 Several explanations have been proposed for the decrease in vascular reactivity during normal pregnancy, such as decreased pressor response to vasoconstrictors, 8 -10 specific alterations within the vascular wall, 11 and an increase in nitric oxide (NO) synthesis. 12,13 Also, Conrad and Vernier 14 have found that the plasma level, metabolic production, and urinary excretion of cGMP, a second messenger of NO and a cellular mediator of vascular smooth muscle relaxation, are increased during pregnancy.…”

Oxytocin does not directly affect vascular tone in vessels from nonpregnant and pregnant rats

“…Pregnancy is a physiological state where vasodilation is necessary to accommodate a 40-50% increase in blood volume required to meet the oxygen and nutritional requirements of the growing uterus and developing fetuses (18,43). This is accompanied by an attenuated responsiveness of maternal vessels to pressor agents (17,29,30,39,40,45) and an enhanced response to vasodilators (28,31). The mechanisms underlying these vascular changes are not clearly understood.…”