RENAL RESPONSES TO ANGIOTENSIN-II INFUSION IN EARLY TYPE-1 (INSULIN-DEPENDENT) DIABETES

被引:6
作者
EADINGTON, DW
SWAINSON, CP
FRIER, BM
SEMPLE, PF
机构
[1] Medical Renal Unit, Royal Infirmary, Edinburgh
[2] Department of Diabetes, Royal Infirmary, Edinburgh
[3] Medical Research Council Blood Pressure Unit, Western Infirmary, Glasgow
关键词
TYPE-1; DIABETES; RENIN ANGIOTENSIN SYSTEM; GLOMERULAR FILTRATION RATE; RENAL PLASMA FLOW; SODIUM EXCRETION;
D O I
10.1111/j.1464-5491.1991.tb01645.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The renal response to infusion of sub-pressor doses of angiotensin 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 angiotensis 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.
引用
收藏
页码:524 / 531
页数:8
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共 43 条
[1]  
Hostetter TH, Troy JL, Brenner BM, Glomerular haemodynamics in experimental diabetes mellitus, Kidney Int, 19, pp. 410-415, (1981)
[2]  
Zatz R., Meyer TW, Rennke HG, Brenner BM, Predominance of haemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy, Proc Natl Acad Sci, 82, pp. 5963-5967, (1985)
[3]  
Zatz R., Dunn BR, Meyer S., Anderson S., Rennke HG, Brenner BM, Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension, J Clin Invest, 77, pp. 1925-1930, (1986)
[4]  
Parving HH, Hommel E., Nielsen MD, Giese J., Effect of captopril on blood pressure and kidney function in normotensive insulin‐dependent diabetics with nephropathy, Br Med J, 299, pp. 533-536, (1989)
[5]  
O'Hare JA, Ferriss JB, Brady D., Twomey B., O'Sullivan DJ, Exchangeable sodium and renin in hypertensive diabetic patients with and without nephropathy, Hypertension, 7, pp. 43-48, (1985)
[6]  
DeChatel R., Weidmann P., Flammer J., Et al., Sodium, renin, aldosterone, catecholamines and blood pressure in diabetes mellitus, Kidney International, 12, pp. 412-421, (1977)
[7]  
Christlieb AR, Kalding A., D'Elia JA, Plasma renin activity and hypertension in diabetes mellitus, Diabetes, 25, pp. 969-974, (1976)
[8]  
Burden AC, Thurston H., Plasma renin activity in diabetes mellitus, Clin Sci, 56, pp. 255-259, (1979)
[9]  
Feldt-Rasmussen B., Mathiesen E., Deckert T., Et al., Central role for sodium in the pathogenesis of blood pressure changes independent of angiotensin, aldosterone and catecholamines in Type 1 (insulin‐dependent) diabetes mellitus, Diabetologia, 30, pp. 610-617, (1987)
[10]  
Christiansen JS, Giese J., Damkjaer M., Parving H-H, The renin‐angiotensin system and kidney function during initial insulin treatment in normal man, Scand J Clin Lab Invest, 48, pp. 451-456, (1988)