No abstract

SUMMARY Isolated kidneys of Dahl salt-sensitive rats (DS) excrete sodium less readily than those of Dahl salt-resistant rats (DR). The collecting tubule is an important source of papillary prostaglandin E2 and is a site of significant sodium reabsorption. We cultured renal papillary collecting tubule cells from 5-week-old, prehypertensive DS and DR on a low salt diet and also after 14 weeks of high salt feeding, and we measured prostaglandin E 2 synthetic capacity. Unstimulated renal papillary collecting tubule cells from 5-week-old DS produced 62 ± 5% less prostaglandin E 2 than did comparable cells from DR (p<0.001). The cells from DS also synthesized less prostaglandin E? after stimulation with the calcium ionophore A23187 (67 ± 6% of control; p < 0.001) or the addition of exogenous arachidonate (74 ± 7% of control; p<0.01). Urinary prostaglandin E? excretion was also diminished in the 5-week-old DS compared with their salt-resistant counterparts (18.1 ± 1.3 vs 23.9 ± 1.7 ng/24 hr; p<0.025). After high salt feeding, the DS became hypertensive but the DR remained normotensive. Renal papillary collecting tubule cells cultured from these DS continued to produce less prostaglandin E 2 than those from control rats, both in the basal state (60 ± 12% of control; p<0.09) and after stimulation with ionophore (62 ± 2% of control; p<0.002). In these older animals, the DS continued to underexcrete prostaglandin E? compared with the DR (29.7 ± 3.2 vs 42.2 ±6.1 ng/24 hr; p < 0.08). The underproduction of prostaglandin E 2 in the papillary collecting tubule of DS may play a role in their inadequate renal natriuretic capacity and contribute to the onset and maintenance of saltinduced hypertension in this strain. (Hypertension 11: 179-184, 1988) KEY WORDS • Dahl rats • prostaglandin Ej • collecting tubule • cell culture D AHL salt-sensitive rats (DS) become hyperten-I sive when fed a diet rich in NaCl, whereas Dahl salt-resistant rats (DR) remain normotensive on a high salt diet. The kidney is of major importance in determining this response. Renal crosstransplantation 12 experiments between DS and DR have shown that salt-sensitivity transfers with the genotype of the donor. Using isolated perfused kidneys, Tobian et al. 3 and Maude and Ko 4 found that, at similar perfusion pressures, DR kidneys display a greater natriuresis than DS kidneys and that, to quantitatively equalize natriuresis, DS kidneys need a higher perfusion pressure. This defective natriuresis probably leads to hypertension through a more complex mechanism than simple volume expansion.

No abstract

No abstract

No abstract