Central role for sodium in the pathogenesis of blood pressure changes independent of angiotensin, aldosterone and catecholamines in Type 1 (insulin-dependent) diabetes mellitus

Abstract

We studied 73 Type 1 (insulin-dependent) diabetic patients, 18 to 50 years of age, with a diabetes duration of more than five years. Group 1: normal urinary albumin excretion below 30 mg per 24 h (n=19); group 2: microalbuminuria, 30-300 mg per 24 h (n=36); and group 3: diabetic nephropathy, above 300 mg per 24 h (n=18). Fifteen non-diabetic persons matched for sex and age served as control subjects. The sodium intake evaluated on the basis of 24-h urine sodium excretion was similar in patients and control subjects. Blood pressure in groups 1 and 2 and control subjects was below 160/95 mmHg. The blood pressure was increased in group 3 as compared with the other groups (systolic/diastolic 161±22/101±9 mmHg vs 131±13/84±10, mean±SD, p<0.0001). Exchangeable sodium was increased in patients (p<0.01) and correlated to the mean blood pressure (n=70, r=0.41, p<0.01). Extracellular volume was increased in patients (p<0.05), whereas plasma volume was normal. Supine serum angiotensin II was suppressed in the patients (p<0.001). A negative correlation was found between mean blood pressure and supine serum aldosterone (n=68, r=-0.24, p<0.05), and exchangeable sodium and aldosterone (n=66, r=-0.36, p<0.002) in all patients. The catecholamine levels were also suppressed or normal in the patients. These data suggest that sodium retention plays a major role and that the aldosterone, angiotensin II and catecholamine levels are suppressed during the blood pressure rise observed in the very early stages of diabetic renal disease. © 1987 Springer-Verlag.