Renal responses to angiotensin II infusion in early type 1 (insulin-dependent) diabetes
Autor: | C. P. Swainson, D. W. Eadington, P. F. Semple, Brian M. Frier |
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Rok vydání: | 1991 |
Předmět: |
Adult
Male medicine.medical_specialty Endocrinology Diabetes and Metabolism Renal function Natriuresis Blood Pressure Kidney Renal Circulation Renin-Angiotensin System Endocrinology Heart Rate Diabetes mellitus Internal medicine Renin–angiotensin system Internal Medicine Medicine Humans Type 1 diabetes business.industry Angiotensin II Effective renal plasma flow medicine.disease medicine.anatomical_structure Diabetes Mellitus Type 1 Renal blood flow Multivariate Analysis business Glomerular Filtration Rate |
Zdroj: | Diabetic medicine : a journal of the British Diabetic Association. 8(6) |
ISSN: | 0742-3071 |
Popis: | The renal response to infusion of sub-pressor doses of angiotension II was examined in nine euglycaemic Type 1 (insulin-dependent) diabetic patients with diabetes of short duration and nine non-diabetic control subjects. Plasma concentrations of angiotensin II and of free insulin were similar in both groups at baseline and during angiotensin II infusion. Glomerular filtration rate (Inutest clearance) fell to a similar extent during angiotensin II infusion in both groups (diabetic 116(SE 5) to 102(5) ml min-1 1.73-m-2; control 113(6) to 100(5) ml min-1 1.73-m-2). There was a large dose-dependent fall in effective renal plasma flow (p-aminohippurate clearance) during angiotensin II infusion which was of similar magnitude in both groups (diabetic; 694(46) to 521(21) ml min-1 1.73-m-2; control 665(41) to 498(30) ml min-1 1.73-m-2). The absolute and the fractional rates of urinary excretion of sodium were both lower in the diabetic group throughout the study, but there was a comparable antinatriuretic response to angiotensin II. Thus, the renal haemodynamic response to angiotensin II infusion is normal in early well-controlled Type 1 diabetes. Differences were found in the renal handling of sodium, which could not be related to altered renal tubular responses to angiotensin II or to peripheral hyperinsulinaemia. |
Databáze: | OpenAIRE |
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