Acute unilateral ureteral pressure elevation impairs renal blood flow autoregulation and redistributes intrarenal blood flow in rats, suggesting a transmural pressure-controlled mechanism.
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Should not change clinical practice; leaves open whether ureteral pressure impairs RBF autoregulation in humans.
The rat kidney autoregulates its blood flow (RBF) when renal arterial blood pressure (RAP) is lowered, but less efficiently than does the dog kidney. We wanted to investigate to what extent acute unilateral elevation of ureteral pressure (UP) in the Sprague‐Dawley rat would interfere with the renal vasodilatory responses elicited by RAP reduction and by intraarterial infusion of acetylcholine (Ach). RBF was significantly better autoregulated before than during UP elevation to 43 mmHg (p<0.001), as measured electromagnetically in an extracorporal flow circuit. However, RBF decreased within the autoregulatory pressure range: Closely similar RBF reductions, 3–4% per 10 mmHg, were obtained both by increasing UP and by decreasing RAP by 10 to 50 mmHg. These RBF reduction did not involve active renal vasoconstriction since maximal dilation by i. a. Ach infusion (∽1.0 μg/min) increased RBF significantly more before and after than during UP elevation (p<0.01). The proportional responses to changes in intra and extra‐vascular pressures therefore suggest that a mechanism controlled by transmural pressure is responsible for RBF autoregulation. UP increase had no effect on contralateral RBF. The effect of UP elevation on intrarenal blood flow distribution, as determined by zonal uptake rates of the diffusible tracer125I‐iodoantipyrine, was studied in a second group of rats at an UP averaging 32 mmHg. Fractional zonal blood flow decreased in outer third (p<0.05) and increased in inner third of the cortex and outer half of the outer medullap<0.05). This redistribution was not detected if cortex was divided in halves only.
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Hope et al. (1982) studied this question.
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