PubMed1975
Isolated kidneys from both "post-salt" normotensive and hypertensive rats were perfused with blood from donor rats at varying pressures. At 130 mm Hg inflow pressure 15 "post-salt normotensive" kidneys put out 0.75 muEq Na/min/g kidney while 14 "post-salt hypertensive" kidneys put out 0.28 mu-Eq Na/min/g (P less than 0.001), a 63% reduction. They also put out 55% less water (P less than 0.002). Thus, if "hypertensive" kidneys are perfused at normal pressures, they put out subnormal amounts of Na and H-2-O. Such Na and H-2-O retention maintains the hypertensive state. Normal Na output in these kidneys was only reached at hypertensive (160) inflow pressures. This shift in the "pressure natriuresis" curve explains in part how some "hypertensive" kidneys maintain hypertension. These "hypertensive" kidneys have grossly abnormal autoregulation curves, each increment of pressure actually producing progressively greater increments of blood flow. Isolated kidneys from Kyoto hypertensive and normotensive rats showed no difference in Na and H-2-O excretion at 130 mm Hg inflow pressure. Thus, a tendency to Na retention demonstrable in the isolated kidney is apparently not supporting Kyoto hypertension. Moreover, isolated kidneys form Kyoto hypertensive rats released significantly lower amounts of renin at all levels of inflow pressure, averaging a 70% lower rate than Kyoto normotensive kidneys (P less than 0.01). Hence, Kyoto hypertension is not supported by a supernormal renin release inherent in the kidney. One can speculate that Kyoto hypertensive rats normally have an elevated sympathetic tone which stimulates release of renin. The denervation which occurs in isolating kidneys might therefore produce a proportionally greater percentage loss of sympathetic influence in these kidneys, which could possibly account for some of their reduced renin release. These Kyoto hypertensive kidneys are apparently not "reset" to maintain hypertension with either Na or renin.