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This Article Full Text Full Text (PDF) All Versions of this Article: 92/3/575    most recent expphysiol.2006.036152v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ebenezar, K. K. Articles by Smith, F. G. Search for Related Content PubMed PubMed Citation Articles by Ebenezar, K. K. Articles by Smith, F. G.

¹ Department of Physiology & Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada

Both prostaglandins (PGs) PGE₂ and PGI₂ 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.

(Received 17 October 2006; accepted after revision 18 December 2006; first published online 18 January 2007)
Corresponding author F. G. Smith: Department of Physiology & Biophysics, Faculty of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada. Email: fsmith{at}ucalgary.ca