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HIGH SALT DIET AMELIORATES EFFECTS OF ANGIOTENSIN CONVERTING ENZYME INHIBITION IN SPONTANEOUSLY HYPERTENSIVE STREPTOZOTOCIN DIABETIC RATS
Author(s) -
Jackson Bruce,
Fabris Bruno,
Paxton Donna,
Franze Linda,
Johnston Colin I.
Publication year - 1990
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1990.tb01312.x
Subject(s) - endocrinology , streptozotocin , medicine , diabetic nephropathy , blood pressure , diabetes mellitus , angiotensin converting enzyme , renin–angiotensin system , excretion , angiotensin ii , chemistry
SUMMARY 1. To dissociate the effects on the development of diabetic renal injury of angiotensin converting enzyme (ACE) inhibition per se , and a reduction in systemic blood pressure, we have studied the effects of chronic ramapril treatment in streptozotocin diabetic spontaneously hypertensive rats, with modulation of the hypotensive effect by a high salt diet. 2. Three weeks following uninephrectomy and induction of diabetes with streptozotocin, spontaneously hypertensive rats were allocated to three treatment groups. Groups 1 and 2 received 1% sodium chloride and Group 3 water as drinking solution. Groups 2 and 3 received 0.4 mg/kg per day ramapril in drinking solution over the subsequent 2 month study period. 3. Sodium chloride drinking solution (1%) completely prevented any hypotensive effect of ramapril. Blood pressure was reduced in Group 3 rats over the entire period of study, when compared with Group 2 rats ( P <0.001). 4. Urinary protein excretion progressively increased in Group 1 and 2 rats, and was significantly reduced ( P <0.001) in Group 3. After 2 months treatment, urinary protein (expressed as mean and s.e.m.) was 160±30 mg/day in Group 1, 240±50 mg/day in Group 2, and 60±11 mg/day in Group 3. 5. Angiotensin converting enzyme inhibition per se was not associated with a reduced protein excretion in diabetic nephropathy, requiring concomitant control of systemic blood pressure to become renoprotective.