The renal microvascular responses of Wistar-Kyoto and spontaneously hypertensive rats to changes in perfusion pressure were compared using a juxtamedullary nephron microvascular preparation perfused in vitro with a physiological salt solution containing 5% albumin. In the spontaneously hypertensive rats, the internal diameters of arcuate and interlobular arteries and the proximal and distal afferent arterioles averaged 307±26, 52±2, 24±0.9, and 22±1.2 ftm, respectively, at 80 mm Hg. They were 18-35% smaller (p<0.05) than the corresponding vessels measured in Wistar-Kyoto rats. In low calcium media, the arcuate and interlobular arteries and the proximal and distal afferent arterioles of spontaneously hypertensive rats exhibited a greater dilation than the vessels of Wistar-Kyoto rats. These observations suggest that the diameters of the preglomerular vasculature of the spontaneously hypertensive rats are reduced because of an elevated vascular tone rather than structural changes narrowing the lumen of these vessels. These results suggest that enhanced vascular tone in the preglomerular vasculature of juxtamedullary nephrons may contribute to the elevated renal medullary vascular resistance and resetting of the pressure-natriuretic relation previously observed in spontaneously hypertensive rats. (Hypertension 1990;16:648-654) R enal transplantation studies have indicated that some form of renal dysfunction underlies the development of genetic hypertension.12 Nevertheless, the factors that contribute to the "resetting of the kidney in hypertension" remain unknown. Numerous differences in renal function of spontaneously hypertensive rats (SHR) and WistarKyoto (WKY) rats have been described; these include an elevated renal vascular resistance, 3 -5 enhanced renal vascular reactivity to vasoconstrictors, 4 -5 enhanced tubuloglomerular feedback response, 6 and structural changes that increase the wall-to-lumen ratio in the renal vasculature.78 Because most of these changes have been identified in the established phase of hypertension, it remains unclear whether these changes are a cause or a consequence of the disease.We recently reported that the pressure-natriuretic response is blunted in SHR and Dahl salt-sensitive rats before the development of hypertension. 910 In the SHR, the abnormality in the pressure-natriuretic response is associated with a reduction in papillary blood flow 11 and renal interstitial hydrostatic pressure. 12 These observations suggest that an elevation in renal medullary vascular resistance may participate in the resetting of the renal function toward higher pressures in SHR.
11The factors responsible for reducing papillary blood flow in SHR are unknown. Medullary blood flow is derived exclusively from the perfusion of deep nephrons. Thus, structural changes that narrow the lumen of the preglomerular vasculature of juxtamedullary nephrons or alterations in the reactivity of these vessels could be responsible for the!, reduction of papillary blood flow in SHR. The recent development of the in ...