Antinatriuretic action of insulin is preserved after angiotensin I converting enzyme inhibition in normal man
| Autor: | D. A. Hepburn, D. W. Eadington, C. P. Swainson |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Adult
Blood Glucose Male medicine.medical_specialty Indoles Lithium (medication) Metabolic Clearance Rate medicine.medical_treatment Natriuresis Angiotensin-Converting Enzyme Inhibitors Lithium Renal Circulation Hyperinsulinism Internal medicine Renin–angiotensin system Perindopril medicine Humans Insulin Transplantation Kidney biology business.industry Angiotensin-converting enzyme Water-Electrolyte Balance medicine.disease Angiotensin II medicine.anatomical_structure Endocrinology Nephrology biology.protein business medicine.drug |
| Zdroj: | Nephrology Dialysis Transplantation. 8:29-35 |
| ISSN: | 1460-2385 0931-0509 |
| DOI: | 10.1093/oxfordjournals.ndt.a092267 |
| Popis: | To examine the potential role for intrarenal angiotensin II in mediating the antinatriuretic action of insulin, seven normal males were studied on three occasions, twice during euglycaemic hyperinsulinaemia (40 mU.m-2.min-1) after double-blind treatment for 1 week with placebo and the converting enzyme inhibitor perindopril, and on a time control day. Lithium carbonate 250 mg was given before each study as an indirect marker of tubular sodium handling. Renal haemodynamics did not change during hyperinsulinaemia. Insulin infusion reduced both the absolute and fractional urinary excretion rates of sodium (P < 0.001) and potassium (P < 0.001); these effects of insulin were not altered after converting enzyme inhibition. Lithium clearance did not change during insulin infusion on either day. The antinatriuretic effect of hyperinsulinaemia is mediated at a tubular site distal to the proximal tubule. The data does not support the hypothesis that intrarenal generation of angiotensin II plays a part in this action of insulin. |
| Databáze: | OpenAIRE |
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