Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats).

Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats). Dahl described a strain of rats with genetically controlled propensities for hypertension. Chronic excess salt feeding increased blood pressure in sensitive (S) rats, whereas resistant rats (R) remain normotensive. We tested the pressure natriuretic function (urinary sodium excretion versus perfusion pressure) in isolated kidneys perfused with a cellular medium: in sodium-restricted normotensive sensitive (S 0 ) and resistant (R 0 ) animals; in sensitive rats receiving a high-salt diet for 3 weeks (S 3 ); and in both S and R animals exposed to excess sodium for 7 weeks (R 7 and S 7 ). The aim of these studies was to determine if a preset alteration of the pressure natriuretic function might be present in S animals prior to the development of hypertension. Systolic blood pressure in S 0 , S 3 , and S 7 animals were 123 ± 4, 136 ± 2, and 162 ± 4mm Hg, respectively, whereas that of R 0 and R 7 were 121 ± 5 and 126 ± 5mm Hg. An increase of the perfusion pressure of isolated kidneys from 105 to 185mm Hg in stepwise fashion resulted in a pressure natriuresis whose slope was similar in R 0 and S 0 animals. Of interest was that the pressure natriuretic function slope of kidneys from R 0 (low sodium) and R 7 (high sodium) rats was as predicted by the Guyton system analysis of normal blood pressure control. Micropuncture of the proximal nephrons demonstrated that the origin of the natriuresis resulted from a site beyond the accessible proximal tubule. Results from S 7 kidneys contrasted with all others in that the natriuretic response was depressed (P Natriurese de pression dans les reins isoles provenant de rats de Dahl sensibles ou resistants a l'hypertension. Dahl a decrit une souche de rats ayant une propension genetique a l'hypertension. L'administration d'une alimentation riche en sel augmente la pression arterielle chez les rats sensibles (S) alors que les rats resistants (R) restent normotendus. Nous avons etudie la natriurese de pression (excretion urinaire de sodium en fonction de la pression de perfusion) dans des reins isoles perfuses avec un milieu cellulaire provenant de rats normotendus S 0 et R 0 soumis a une restriction de sodium, de rats sensibles ayant recu une alimentation riche en sel pendant trois semaines (S 3 ) et de rats S et R exposes a un exces de sel pendant 7 semaines (R 7 et S 7 ). Le but de ces etudes est d'etablir l'existence eventuelle d'une modification de la relation pression natriurese avant le developpement de l'hypertension. Les pressions systoliques des rats, S 0 , S 3 , et S 7 etaient de 123 ± 4, 136 ± 2, et 162 ± 4mm Hg, respectivement, alors que celles de R 0 et R 7 etaient de 121 ± 5 et 126 ± 5mm Hg. Une augmentation de la pression de perfusion de reins isoles de 105 a 185mm Hg, par paliers, a eu pour resultat une natriurese de pression dont la pente etait la meme chez R 0 et S 0 . Il est interessant de remarquer que la pente de cette relation pour les reins R 0 (sodium bas) et R 7 (sodium eleve) est celle qui est prevue par l'analyse de Guyton du controle normal de la pression arterielle. Des microponctions des nephrons proximaux ont montre que l'origine de la natriurese est en aval du tuble proximal accessible. Les resultats des reins S 7 ont ete differents de tous les autres en ce sens que la reponse natriuretique a ete deprimee (P