THE DOPAMINURIC RESPONSE TO HIGH-SALT DIET IN INSULIN-DEPENDENT DIABETES-MELLITUS AND IN FAMILY HISTORY OF HYPERTENSION

Citation
S. Rudberg et al., THE DOPAMINURIC RESPONSE TO HIGH-SALT DIET IN INSULIN-DEPENDENT DIABETES-MELLITUS AND IN FAMILY HISTORY OF HYPERTENSION, Pediatric nephrology, 11(2), 1997, pp. 169-173
Citations number
32
Categorie Soggetti
Pediatrics,"Urology & Nephrology
Journal title
Pediatric nephrology
ISSN journal
0931041X → ACNP
Volume
11
Issue
2
Year of publication
1997
Pages
169 - 173
Database
ISI
SICI code
0931-041X(1997)11:2<169:TDRTHD>2.0.ZU;2-W
Abstract
Alterations in the renal dopamine [DA] system have been suggested to c ontribute to the development of hypertension and diabetic nephropathy. To identify early abnormalities in renal handling of DA and sodium we challenged 16 normotensive patients with uncomplicated insulin-depend ent diabetes (IDDM), 18 normotensive nondiabetic subjects with familia l borderline hypertension, and 16 healthy controls, 14-29 years old, w ith a high-sodium diet (HSD). Systolic blood pressure was slightly hig her in subjects with familial borderline hypertension than in the othe r groups on a normal sodium diet (NSD) (P < 0.05). Blood pressure and 24-fi urinary measurements were performed on a NSD and after 3 days on a HSD. Twenty-four-hour urinary DA excretion was similar in all group s on NSD. A significant rise in DA excretion was noted after HSD in co ntrol subjects (P < 0.01), but not in subjects with a family history o f hypertension or with IDDM. Urinary sodium excretion increased in all groups. A correlation between the change in DA and sodium/creatinine ratio after HSD was seen in healthy controls (r = 0.57, P = 0.02) but not in those with familial borderline hypertension (r = 0.18, P = 0.47 ) or with IDDM (r = 0.40, P = 0.15). A rise in systolic (but not diast olic) pressure was noted only in the IDDM group after HSD (P = 0.02). In conclusion, an impairment in the renal DA and sodium system can be detected early in IDDM and in individuals with familial hypertension. We speculate that this impairment may contribute to the development of hypertension and microvascular disease in both conditions.