Received October 17, 2006
Revised November 23, 2006
Accepted after revision December 18, 2006

¹ University of Calgary
² Marshad University of Iran

^* To whom correspondence should be addressed. E-mail: fsmith{at}ucalgary.ca.

	Abstract

Both prostaglandins (PG’s) PGE2 and PGI2 can act as renal vasodilators, these effects being exacerbated when the renin-angiotensin system is activated. Therefore, we hypothesized that PG’s 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 PG’s in modulating systemic and renal haemodynamics was investigated in two groups of conscious developing lambs aged ~oneand ~sixweeks, post natally. Arterial pressure (AP), venous pressure (VP) and renal blood flow (RBF) were measured for 5 min before (Control) and for 20 min after intravenous (I.V.) injection of vehicle (experiment one) and after 24 h, the non-selective cyclooxygenase inhibitor indomethacin (1 mg/kg, experiment two). Heart rate (HR) 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 MAP and pulse interval as well as a marked increase in RVR. The aforementioned responses to indomethacin were, however, transient with baseline levels being reached within minutes. Although the hypothesis that PG’s play a greater role in modulating renal haemodynamics early in life is not supported, these data do provide evidence that endogenously produced PG’s modulate systemic and renal haemodynamics during postnatal maturation. It is apparent, however, that other vasoactive factors must be rapidly recruited which serve to buffer the circulatory responses to removal of vasodilatory PG’s in the developing newborn.

Key Words: Neonate, Prostaglandin, Vasoconstriction