Aggravation of hypertension in spontaneously hypertensive rats by Heymann nephritis.
1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.
D000818:Animals; D001794:Blood Pressure; D005260:Female; D006973:Hypertension / Q000150:complications* / Q000235:genetics; D009206:Myocardium / Q000473:pathology; D009393:Nephritis / Q000150:complications* / Q000652:urine; D009929:Organ Size; D011507:Proteinuria; D051381:Rats; D012964:Sodium / Q000652:urine; D013997:Time Factors
D012964:Sodium