Determinants of Renal Vascular Resistance in the Dahl Strain of Genetically Hypertensive Rat

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 1980-05, Vol.2 (3), p.274-280
• Main Authors: FINK, GREGORY D, TAKESHITA, AKI, MARK, ALLYN L, BRODY, MICHAEL J
• Format: Article
• Language: English
• Subjects: Animals; Blood Flow Velocity; Blood Pressure - drug effects; Female; Hypertension, Renal - genetics; Hypertension, Renovascular - genetics; Kidney - blood supply; Kidney - physiology; Rats - genetics; Sodium - administration & dosage; Sodium - pharmacology; Sympathetic Nervous System - physiology; Vascular Resistance
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.hyp.2.3.274

SUMMARY Hypertension-resistant (R) rats of the Dahl strain remain normotenslve on diets containing excessive sodium chloride, while hypertension-sensitive (S) rats rapidly become hypertensive when eating the same diet. In the present study, renal hemodynamlcs were investigated in Dahl rats eating normal or high salt chow for 4 weeks. The R rats eating sodium-enriched cbow were found to have significantly lower renal vascular resistance (RVR) than R rats on normal chow; RVR was identical in S rats on either diet. The reason for the failure of S kidneys to exhibit vasodilation during high salt ingestion was explored by examining renal vascular responses to interruption of the renal sympathetic nerves, renal sympathetic nerve stimulation (SNS), and to several vasoactive agents. Changes in RVR to nerve section and to SNS were similar in both strains regardless of diet Renal vascular responses to Intraarteritl norepinephrine were suppressed significantly by high salt intake only in the R rats. Changes in RVR to lntraarterlal angiotensin II were uniformly greater in S than in R rats, but were not altered by salt intake in either strain. Renal vasodilation in response to intraarterial acerylcholine was reduced in R rats on high salt intake, but was not affected by salt intake in S rats. It is concluded that S rats exhibit inappropriately high renal vascular tone during ingestion of excessive salt, and that this alteration is not the result of increased neurogenic activity or increased vascular reactivity to angiotensin II or norepinephrine.