Resetting of pressure-natriuresis and frusemide sensitivity in spontaneously hypertensive rats.

We compared pressure-natriuresis in isolated perfused kidneys of spontaneously hypertensive rats (SHR), and age-matched controls, and studied the effect of frusemide on sodium excretion. Okamoto SHR and age-matched Wistar-Kyoto controls (WKY) were used. Conscious BP was measured in a tail artery cannulated before the experiment. Isolated kidneys were perfused at 37 degrees C and glomerular filtration rate, urinary sodium excretion (UNaV) and percentage sodium reabsorption (%TNa) were measured as mean perfusion pressure was increased in steps from 100 to 180 mmHg and repeated after addition of frusemide. At all perfusion pressures GFR and UNaV were lower in SHR and %TNa higher, consistent with a 50 mmHg rightward shift of the pressure-natriuresis relationship in SHR. However, at intrarenal perfusion pressure equal to MBP, sodium excretion was the same (2.9 microEq/min/g WKY; 2.7 microEq/min/g SHR). Subsequent response to frusemide was markedly reduced in SHR. We conclude that resetting of pressure-natriuresis in SHR compensates exactly for increased renal perfusion pressure. The mechanism by which these are so precisely linked is not known, nor is the reason for the blunted sensitivity to frusemide in SHR, but it is possible that Na-K-Cl cotransport in Henle's loop may be altered in this genetic model of hypertension.