Relationships among natriuresis, atrial natriuretic peptide and insulin in insulin-dependent diabetes

摘要

Relationships among natriuresis, atrial natriuretic peptide and insulin in insulin-dependent diabetes. Insulin-dependent diabetic patients have a large exchangeable body sodium pool, secondary to sodium retention. The pathogenesis of impaired natriuresis in insulin dependent diabetes remains to be elucidated. The present study examines the role of hyperinsulinemia, impaired atrial natriuretic release, and resistance to atrial natriuretic peptide action in determining sodium retention in normotensive and hypertensive insulin-dependent diabetic patients. Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 16 mmol/day; mean SE) during conventional insulin treatment (daily plasma glucose: 11.6 1.2 mmol/liter; daily plasma insulin: 27 3 U/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 12, P 2 min) than in control subjects (199 14 to 341 22, P < 0.01). Natriuretic action of atrial natriuretic peptide was similarly impaired in a group of eighteen hypertensive insulin-dependent diabetic patients in comparison with a matched group of seven hypertensive control patients. Angiotensin converting enzyme inhibitor treatment in these hypertensive diabetic patients decreased extracellular liquid volume and improved natriuretic response to atrial natriuretic peptide. We conclude that refractoriness to natriuretic action rather than impaired release of atrial natriuretic peptide can further deteriorate sodium retention in insulin dependent diabetes. This altered hormonal behavior could be primarily due to insulin-induced sodium retention and extracellular liquid volume expansion.