Acute hypoxemia causes a decrease in glomerular filtration rate (GFR) and renal blood flow (RBF) in newborns. These changes are partly mediated by local-acting vasoactive factors. We have previously shown that bradykinin (BK) has a vasodilatory role in the basic regulation of neonatal hemodynamics. The purpose of the present study was to evaluate whether BK can modulate the severe renal vasoconstriction associated with hypoxemia in the newborn rabbit. The effect of systemic hypoxemia (PaO2 approximately 40 mmHg) on renal function was investigated in 9 newborn rabbits (controls) and in 8 animals in which BK-B2 receptors were blocked by Hoe 140 (300 microg/kg subcutaneously), given prior to the induction of hypoxemia. The studies were performed under pentobarbital anesthesia at the age of 5-9 days. In control animals, acute hypoxemia caused a significant decrease in GFR and RBF and an increase in renal vascular resistance. Similar glomerular hemodynamic changes were observed in BK-B2 receptor-blocked newborn rabbits. These results indicate that BK does not play a significant role in the renal vascular changes of the hypoxemic-stressed newborn.

The aim of this study was to investigate the acute, short-term effects of the intravenous (i.v.) administration of magnesium (Mg) sulfate on renal function in the newborn rabbit. Eight anesthetized and mechanically ventilated, normoxemic, newborn New Zealand white rabbits were studied. We measured mean arterial blood pressure (MAP), urine volume (V), glomerular filtration rate (GFR), renal plasma flow (RPF) and calculated renal blood flow, filtration fraction (FF) and renal vascular resistance (RVR) under control conditions and in two experimental periods after the i.v. Mg sulfate load. Mg sulfate administration in a dose 100 mg/kg followed by 50 mg/kg/h caused a significant fall (p < 0.001) in MAP, GFR and RPF, whereas the RVR increased (p < 0.01). FF did not change significantly (p: NS/0.05) and V remained constant. These results show that the acute i.v. administration of Mg sulfate to newborn rabbits causes systemic vasodilatation with a fall in MAP. The increase in RVR, without consistent change in FF, suggests that the renal vasculature of the ‘immature’ neonatal rabbit reacts to these changes by preferential afferent arteriolar vasoconstriction.

Angiotensin-converting enzyme (ACE) inhibitors exert their effects by inhibiting angiotensin II (AII) production, but also by inhibiting bradykinin (BK) degradation. In order to clarify whether BK is involved in the systemic effects of ACE inhibition in the newborn period, we investigated the effect of perindoprilat (20 μg/kg i.v.) in newborn rabbits, with or without the blockade of BK β₂-receptors (Hoe 140, 300 μg/kg s.c.). The bolus infusion of perindoprilat resulted in a marked fall in mean arterial blood pressure (MBP) and a slight decrease in heart rate. BK receptor blockade had no effect on the perindoprilat-induced hypotension but the negative chronotropic effect of ACE inhibition was partly prevented by pretreatment with Hoe 140. We therefore conclude that BK is not involved in neonatal blood pressure regulation but that the ACE inhibition-induced neonatal bradycardia is at least partly BK- mediated.