The renal medulla and mechanisms of hypertension in the spontaneously hypertensive rat.
A significant number of offspring from brother-sister matings of NIH-Okamoto-Aoki spontaneously hypertensive rats (SHRs) were found to be normotensive at 20 weeks of age. Over 20% of the animals that were hypertensive at this age had mild-to-moderate unilateral hydronephrosis at the time of sacrifice. In over 90% of the rats that did not develop hypertension spontaneously, ligation of one ureter raised blood pressure above 150 mm Hg within 2 weeks. In those rats made hypertensive by obstructing one ureter and in those that developed hypertension with accompanying naturally occurring hydronephrosis, subcutaneous implants of fragmented renal medulla from unrelated normal rats decreased blood pressure to normotensive levels. In contrast, medullary implants had no significant effect in rats developing hypertension spontaneously without hydronephrosis. Renal inner medullary plasma flow was low in the obstructed kidneys of hydronephrotic hypertensive SHRs but was elevated in the kidneys of nonhydronephrotic hypertensive SHRs. The hypertension in hydronephrotic SHRs appears to be related to an impairment of the antihypertensive function of the renal medulla. Such an impairment of medullary antihypertensive function does not appear to play a significant role in the hypertension in SHRs without hydronephrosis.
D000818:Animals; D006869:Hydronephrosis / Q000150:complications; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology* / Q000662:veterinary; D007668:Kidney / Q000473:pathology / Q000503:physiopathology*; D007672:Kidney Cortex / Q000637:transplantation; D007679:Kidney Medulla / Q000098:blood supply / Q000503:physiopathology* / Q000637:transplantation; D008026:Ligation; D051381:Rats; D012376:Rodent Diseases / Q000503:physiopathology; D014184:Transplantation, Homologous; D014513:Ureter / Q000601:surgery