ABSTRACT. The release of vasopressin, renin, and catecholamines by the fetus during either maternal or fetal hypotension was examined in chronically catheterized fetal lambs. Nitroprusside was infused intravenously for 1 h into seven pregnant ewes (maternal hypotension) or nine fetal lambs (fetal hypotension); the rates were adjusted to achieve a 15 to 30% decrease in mean blood pressure. During maternal hypotension, mean f S E vasopressin in maternal plasma increased from 1.2 f 0.2 pg.ml-' to 208 f 153 pg.ml-' and plasma renin activity increased from 1.5 f 0.3 ng.ml-'. h-' to 6.6 f 1.6 ng.ml-'. h-'. Fetal vasopressin and plasma renin activity also increased during the same interval from 1.1 f 0.3 to 16.9 +. 7.5 pg.ml-' and 3.7 f 1.1 to 10.5 f 2.85 ng.ml-'.h-', respectively; but no changes were observed in fetal blood pressure, heart rate, or acid base status. During fetal hypotension, mean vasopressin in fetal plasma increased from 4.3 f 3.4 pg. ml-' to 1054 f 772 pg.ml-', plasma renin activity increased from 5.7 f 2.2 ng . ml-' to 22.2 f 7.1 n g ml-' . h-', and total catecholamines from 174 f 58 pg . ml-' to 810 f 416 p g ml-'. There was no change in fetal heart rate, acid base status, osmolality, or sodium concentration. The fetus became and remained hypertensive for at least 1 h after the end of infusion. This prolonged hypertension was associated with elevated levels of vasopressin and plasma renin activity. Peak vasopressin levels were proportional to the total nitroprusside dose in both the ewe and fetus (maternal r = 0.796, fetus r = 0.870). These experiments indicate that as in the adult, vasopressin and the reninangiotensin system in the fetus are stimulated by euvolemic hypotension and may play an important role in the maintenance of fetal blood pressure during an hypotensive challenge. We speculate that the prolonged rebound hypertension represents immaturity of the fetus to fine tune the regulation, release, or metabolism of vasoactive mediators. More likely, the hypertension and elevated hormone levels represent homeostatic mechanisms to combat the nitroprusside-induced diminished cardiac output. Lastly, fetal release of vasopressin, renin-angiotensin, and norepinephrine during maternal hypotension suggests that they are sensitive indicators of early fetal compromise.
7The fetus may be compromised by episodes of maternal hypotension (postural changes, regional anesthesia, placenta previa, etc.) or fetal hypotension (cord occlusion, fetal blood loss secondary to abruptio placentae, etc.) (1). In adults of several species, hypotension is known to stimulate several vasoactive systems which act to restore blood pressure towards normal values (2-8).The ability of the fetus to similarly withstand hypotension may have a significant influence on subsequent short-term and longterm outcome. The present studies were undertaken to determine the fetal response to both maternal and fetal hypotension with respect to fetal release of vasopressin, renin, and catecholamines in the maintenance of fetal blood pressur...