Abstract
THE rabbit kidney has a high capacity for prostaglandin biosynthesis. The major renal prostaglandin released in response to various stimuli is PGE2, a vasodepressor prostaglandin1 thought to have a role in the regulation of intrarenal blood flow2. Although renal prostaglandin synthesis may initiate a reduction in vascular resistance of the kidney in response to reduced perfusion pressure, it has not been possible to establish a functional role for renal prostaglandins as mediators of increased vascular resistance evoked by augmented renal perfusion pressure. An increase in renal resistance, if related to changes in the rate of synthesis of endogenous substances, implies the biosynthesis of a vasoconstrictor or suppression of the basal production of a vasodepressor material. Unilateral ureteral obstruction (model of hydronephrosis) in the dog, rat and rabbit is initially associated with a decrease in renal resistance which is followed by a fall in GFR and renal blood flow3,4 by 24 h post-occlusion. The initial renal vasodilator phase may be associated with enhanced renal basal PGE2 synthesis and markedly facilitated PG release in response to hormone stimulation5. Here we report the observation that the ureter-obstructed kidney may be producing a natural vasoconstrictor material.
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MORRISON, A., NISHIKAWA, K. & NEEDLEMAN, P. Unmasking of thromboxane A2 synthesis by ureteral obstruction in the rabbit kidney. Nature 267, 259–260 (1977). https://doi.org/10.1038/267259a0
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DOI: https://doi.org/10.1038/267259a0
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