Both prostaglandins (PGs) PGE 2 and PGI 2 can act as renal vasodilators, these effects being exacerbated when the renin-angiotensin system is activated. Therefore, we hypothesized that PGs would play a more predominant role in modulating renal haemodynamics in the newborn period, when the renin-angiotensin system is activated. To this end, the role of endogenously produced PGs in modulating systemic and renal haemodynamics was investigated in two groups of conscious lambs aged ∼1 and ∼6 weeks. Arterial pressure, venous pressure and renal blood flow were measured for 5 min before (control) and for 20 min after intravenous injection of vehicle (experiment 1). Twenty-four hours later, this protocol was repeated with intravenous injection of the non-selective cyclo-oxygenase inhibitor indomethacin (1 mg kg −1 , experiment 2). Heart rate was calculated from the systolic peak of the arterial pressure waveform, and renal vascular resistance (RVR) was calculated from the measured variables. In response to indomethacin but not vehicle, in both age groups of lambs there was an increase in mean arterial pressure and pulse interval, as well as a marked increase in RVR. These responses to indomethacin were, however, transient, with baseline levels being resumed within minutes. Although the hypothesis that PGs play a greater role in modulating renal haemodynamics early in life is not supported, these data do provide evidence that endogenously produced PGs modulate systemic and renal haemodynamics during postnatal maturation. It is apparent, however, that other vasoactive factors must be rapidly recruited in order to buffer the circulatory responses to removal of vasodilatory PGs in the developing newborn.

Previously, we showed that ET‐1 elicits no renal vasoconstriction when administered to conscious newborn lambs (Smith et al. 2002, 2005). To test the hypothesis that vasodilatory prostaglandins modulate the renal haemodynamic response to ET‐1 during postnatal maturation, experiments were carried out in two age groups of conscious, chronically instrumented lambs: group I (8 – 17 days; n=4) and group II (32 – 57 days; n=6). Mean arterial (MAP) and venous pressures (MVP) as well as renal blood flow (RBF) were measured at 20 sec interval for one‐min before (Control, C) and five‐min after intra‐arterial (I.A.) injection of ET‐1 (250 ng/kg) both before and after intra‐venous (I.V.) injection of vehicle (Veh, experiment one) and the non‐selective cyclo‐oxygenase inhibitor, indomethacin (Indo, 1 mg/kg, experiment two). Renal vascular resistance (RVR) was calculated as (MAP‐MVP)/RBF. In group I, RVR was 41.1±9.4 mmHg·mL−1·min·g during C and 33.3±4.2 mmHg·mL−1·min·g at 1 min after ET‐1. In group II, RVR increased from 32.9±7.0 to 58.3±40.7 mmHg·mL−1·min·g at 1 min after ET‐1 and 61.3±33.8 mmHg·mL−1·min·g at 2 min. Neither Veh nor Indo had any significant effect on these RVR responses to ET‐1 in either group. Therefore, prostaglandins do not appear to modulate the renal haemodynamic responses to ET‐1 in conscious lambs during postnatal maturation.

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