Developmental aspects of the renal response to hypoxemia in the lamb fetus.

Abstract

SUMMARY The effects of fetal hypoxemia on renal hemodynamics and renal function were studied in two groups of chronically catheterized young (<120 days of gestation) and near-term lamb fetuses (>130 days). Fetal hypoxemia produced, in both groups, a significant decrease in renal blood flow (RBF) and a significant increase in the filtration fraction. However, the glomerular filtration rate (GFR) did not change significantly, suggesting that the renal vasoconstriction associated with fetal hypoxemia was more important at the efferent than at the afferent arteriolar level. In the group of near-term fetuses, the decrease in RBF correlated closely with changes in plasma renin activity (PRA) (r = -0.77). No changes in PRA were observed during hypoxemia in the group of young fetuses. After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF 2a ) was observed in near-term fetuses but not in young fetuses. It also was demonstrated that fetal hypoxemia produced a significant increase in fetal plasma concentrations of vasopressin associated with an antidiuresis in all but one near-term fetus and in 50% of the young fetuses, suggesting that the ability of the fetal kidney to reabsorb free water is more developed in near-term fetuses. Finally, fetal hypoxemia had no effect on mean arterial pressure and heart rate in young fetuses; however, in nearterm fetuses, a significant increase in blood pressure and a decrease in heart rate were observed. In summary, it appears that the response of the fetal kidney to hypoxemia depends on the degree of fetal maturation. Circ Res 48: 128-138. 1981

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

“…Some studies show UO to fall during hypoxia (3 h: Brace, Wlodek, McCrabb & Harding, 1994;30 min: Nakamura et al 1985), while others show no significant change after approximately 1 h of hypoxia (Robillard et al 1981;Wlodek et al 1989). When hypoxia is prolonged (24 h), UO is greater than control levels (Brace et al 1994;Cock, Wlodek, Hooper, McCrabb & Harding, 1994).…”

“…2) There have previously been a number of studies on the effects of hypoxia on fetal RBF in animals and man, but their results are conflicting. On the one hand, low umbilical Pa02 has been linked to a high impedance to renal arterial flow in human fetuses (Vyas, Nicolaides & Campbell, 1989), and experimentally induced acute hypoxia in fetal sheep is reported to produce a fall in RBF (Cohn, Sacks, Heymann & Rudolph, 1974;Robillard et al 1981Robillard et al , 1986Nakamura et al 1985) and in some instances a rise in RVR (Robillard et al 1981(Robillard et al , 1986 Reuss, Parer, Harris & Kreuger, 1982). Furthermore, elevated fetal Pa C02 levels cause a fall in RBF (Beguin, Dunnihoo & Quilligan, 1974).…”

Fetal renal artery flow and renal echogenicity in the chronically hypoxic state

“…During hypoxemia, the renal blood flow fell by 25-50% as compared to the baseline values, but the exact mechanism of this reduction has not been elucidated [17]. This would imply that, instead of a local vasoconstriction of the renal vasculature, the fetal renal blood flow may be maintained by a combination of mechanisms including an increase in arterial pressure and the intrarenal action of various metabolites, which ultimately induce a similar hemodynamic change [18]. A direct relationship has been reported between hypoxia and the renal artery pulsatility index (e.g., resistance) [19].…”

Plasma vasopressin, renin and catecholamines during nitroprusside-induced hypotension in the newborn lamb

“…However the rate of rise in the levels suggest that this more likely is due to stimulation of the neurohypophyseal, sympatho adrenal and renin-angiotensin systems in order to maintain blood pressure [2,8,10,11,13,17,29,32]. Since neither pHa, PaO 2 , plasma sodium or osmolality were significantly affected by nitroprusside, hypoxia and hemoconcentration can be ruled out as possible causes for the release of these vasoactive mediators [4,5,7,26,32]. Gavras suggests that in the adult, the sympathetic nervous system is more involved in the maintenance of blood pressure whereas vasopressin and renin are important back-up mechanisms [9].…”