Salt excretion and vascular resistance of perfused kidneys of Dahl rats.
We used a cell-free, 5% albumin-containing bicarbonate saline solution to perfuse kidneys of salt-sensitive (S) and salt resistant (R) rats derived from Dahl's original strains. The animals had been maintained on diets whose salt content was either 8% ((+)Na) or 0.4% ((-)Na). On these regimens only S(+)Na rats become hypertensive. Glomerular filtration rate (GFR), urinary sodium excretion (NaE), renal vascular resistance (RVR), and filtration fraction were measured as perfusate pressure (P) was increased in stepwise fashion from the 80-100 to the 140-160 mm Hg range. Pressure-GFR and pressure-natriuresis curves for the S(-)Na kidneys were displaced to the right of R, so that for any given value of P both GFR and NaE were significantly less for S(-)Na than for R kidneys. Kidneys from hypertensive (S(+)Na) animals had even more markedly impaired filtration and salt excretion. Although R and S(-)Na kidneys had nearly the same RVR at the lowest perfusate pressures, only the S kidney showed an autoregulatory rise in RVR as perfusate pressure was increased. Filtration fraction did not change, so the rise in resistance probably reflects chiefly afferent arteriolar constriction. Thus, in comparison with R, perfused S kidneys show an intrinsic defect in salt excretion ascribable to a reduced filtered sodium load. The rightward shift of their pressure-GFR curves may be due to an exaggerated afferent arteriolar vasoconstrictor response to increase in perfusion pressure.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004039:Diet, Sodium-Restricted; D004351:Drug Resistance; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000502:physiology*; D009318:Natriuresis; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000008:administration & dosage / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects
D012964:Sodium