Sympathoadrenal and Renin-Angiotensin Systems in the Development of Two-Kidney, One Clip Renal Hypertension in Rats

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 2; no. 6; pp. 723 - 731
• Main Authors: ANTONACCIO, MICHAEL J, FERRONE, RONALD A, WAUGH, MARGARET, HARRIS, DON, RUBIN, BERNARD
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.11.1980
• Subjects: Adrenal Glands - physiopathology; Adrenal Medulla - surgery; Angiotensin II - physiology; Animals; Blood Pressure - drug effects; Captopril - therapeutic use; Constriction; Hydroxydopamines - therapeutic use; Hypertension, Renal - etiology; Hypertension, Renal - therapy; Male; Rats; Renal Artery; Renin - physiology; Sympathetic Nervous System - physiopathology
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.hyp.2.6.723

SUMMARY The relative roles of tbe sympathetic nerrous system and renin-angiotefisin system in the development of two-kidney renal hypertension were studied using four groups of ratsGroup I = vehicle control; Group II = 6-OH-dopamine (2 weeks prior to renal clipping then weekly throughout the study); Group III = adrenal medullectomy plus vehicle; Group IV = o-OHndopamlne plus adrenal medullectomy. Six weeks after clipping of a single renal artery, plasma renln activity (PRA) was comparably elevated in all groups. However, mean blood pressure (MBP) of Group II was lower than that of Group I controls (154.7 ± 6.8 vs 1973 ± 6.6 mm Hg respectively). Tbe MBP of Group III (207.0 ± 5.2 mm Hg) was not different from that of Group I whereas in Group IV (134.2 ± 18.0 mm Hg) it was markedly lower. All groups of rats were given a single dose of captopril (30 mg/kg p.o.) to inhibit the renin-angiotensin system. Despite differences in starting MBP, captopril caused similar reductions (38-50%) of MBP and increases in PRA in all groups. Similar results were obtained in two-kidney renal hypertensive rats with hypertension of 12 weeksʼ duration. It is concluded that the sympathetic nervous system does not contribute to the elevated PRA in two-kidney renal hypertensive rats but does contribute significantly to the development of hypertension In this model.