Post-stenotic arterial pressures, renal haemodynamics and sodium excretion during graded pressure reduction in conscious rats with one- and two-kidney coarctation hypertension

Abstract

Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analagous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40 +/- 4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141 +/- 6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32 +/- 0.40 to 1.41 +/- 0.28 ml/min; P less than 0.01; glomerular filtration rate (GFR), 1.56 +/- 0.18 to 0.42 +/- 0.33 ml/min, P less than 0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.