Angiotensin II-dependent hypertension in rats with reduced kidney mass at the onset of diabetes

Modesto A. Rojas, Tracy D. Bell, Cassandra Fleming, Hicham Labazi, Michael W. Brands

Research output: Contribution to journalConference abstractpeer-review

Abstract

We have reported consistently that onset of diabetes in L-NAME treated rats causes significant hypertension that is associated with the failure of GFR to increase. Subsequently, we showed that reduced renal mass (RRM) also prevented GFR from increasing during the onset of diabetes, and onset of diabetes in those rats caused hypertension associated with an increase in plasma renin activity. This study tested the role of the renin-angiotensin system in mediating the diabetes-induced hypertension in rats with RRM. RRM was induced by surgical ablation of the poles of the left kidney. Two weeks later, the right kidney was removed during the surgery in which chronic artery and vein catheters were implanted. Total renal mass reduction was approximately 70%. RRM rats were divided into Control (C, n=5) and Captopril (CP, n=4; 14μg/kg/min, iv.) groups. Baseline MAP (measured 18 hr/day) averaged 97±4 and 79±4 mmHgin the C and CP groups, respectively. By the third day after induction of diabetes with STZ(40mg/kg,iv.), MAP had increased to 109±2 mmHg in the C group and was 79±5 mmHg in the CP rats. MAP remained elevated in the C rats, similar to our previous study, and averaged112±4 mmHg (~15 mmHg above baseline) on day 7 of diabetes. In the CP rats, on the other hand, MAP did not increase during diabetes, averaging 79±2 mmHg over the last 3 days of diabetes. Insulin replacement (iv.) was begun after 7 days of diabetes, and by day 4 MAP averaged 103±2 and 71±10 mmHg in the C and CP groups, respectively. GFR averaged1.3±0.2 and 1.0±0.1 ml/min in the C and CP groups during baseline and did not change in either group during the diabetic or insulin replacement periods. There also were no significant differences in sodium excretion between the groups. These results indicate that the renin-angiotensin system is required for diabetes to cause hypertension in rats with reduced renal mass, and also support our hypothesis that an inability of GFR to increase early in diabetes may lead to an angiotensin-II dependent increase blood pressure.
Original languageEnglish
Pages (from-to)558-559
Number of pages2
JournalHypertension
Volume44
Issue number4
DOIs
Publication statusPublished - 31 Oct 2004
Event58th Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research in Association with the Council on Kidney in Cardiovascular Disease - Chicago, United States
Duration: 9 Oct 200412 Oct 2004

Keywords

  • diabetes
  • hypertension
  • reduced renal mass

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