OCTREOTIDE, A SOMATOSTATIN ANALOG, REDUCES INSULIN-SECRETION AND INCREASES RENAL NA+ EXCRETION IN LEAN ESSENTIAL HYPERTENSIVE PATIENTS

被引:10
作者
FERRI, C
DEMATTIA, G
BELLINI, C
LAURENTI, O
BRAVI, C
BALDONCINI, R
BONAVITA, MS
SANTUCCI, A
BALSANO, F
机构
[1] University of L'Aquila. Department of Internal Medicine (AS), Rome
[2] University "La Sapienza" Institute of I Clinica Medica, Andrea Cesalpino Foundation, Rome
关键词
INSULIN; HYPERINSULINEMIA; SOMATOSTATIN; HYPERTENSION; OCTREOTIDE; SODIUM EXCRETION;
D O I
10.1093/ajh/6.4.276
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
The influence of insulin on renal Na+ excretion is still subject to debate. In order to evaluate the effect of insulin suppression on Na+ excretion, 20 never-treated essential hypertensive men and 8 normotensive men were studied. All subjects had a body mass index <27 kg/m2. Both the glucose and the lipid metabolisms were normal. After 2 weeks under normal NaCl intake (120 mEq NaCl daily), either octreotide, a somatostatin analog, or vehicle were infused in a forearm vein during acute volume expansion (0.30 mL/kg/min isotonic saline given intravenously over a period of 30 min). A double-blind randomized cross-over design was followed, and each subject was given both infusions at a 1 week interval. Blood and urine samples were taken at times - 60, 0, 30, 60, 90, 120, 180, 240, and 300 min. Our data showed that octreotide significantly lowered insulin levels in both hypertensives (from 12.2 +/- 2.4 muU/mL at time 0 to undetectable values at time 30 and 60 min) and normotensives (from 11.5 +/- 2.8 muU/mL at time 0, to undetectable values at time 30 and 60 min). Compared to saline infusion alone, octreotide significantly increased Na+ excretion in both hypertensives and normotensives (saline + octreotide v saline alone P < .05 at time 60 and 90 min). In conclusion, octreotide enhanced the natriuretic response to intravenous Na+ load in both hypertensives and normotensives. The increase in urinary Na+ was accompanied by a significant decrease in plasma insulin levels.
引用
收藏
页码:276 / 281
页数:6
相关论文
共 19 条
[1]  
Reaven G.M., Role of abnormalities of carbohydrate and lipoprotein metabolism in the pathogenesis and clinical course of hypertension, J Cardiovasc Pharmacol, 15, pp. S4-S7, (1990)
[2]  
Santucci A., Ferri C., Insulin resistance and essential hypertension: Pathophysiologic and therapeutic implications, J Hypertens, 10, pp. S9-S15, (1992)
[3]  
Ferrannini E., Buzzigoli G., Bonadonna R., Et al., Insulin resistance in essential hypertension, N Eng J Med, 317, pp. 350-357, (1987)
[4]  
Modan M., Halkin H., Almog S., Et al., Hyperinsulinemia. A link between hypertension, obesity, and glucose tolerance, J Clin Invest, 75, pp. 809-817, (1985)
[5]  
Liang C.S., Doherty J.U., Faillace R., Insulin infusion in conscious dogs: Effects on systemic and coronary haemodynamics, regional blood flows, and plasma catecholamines, J Clin Invest, 69, pp. 1321-1336, (1982)
[6]  
Landsberg L., Hyperinsulinemia: Possible role in obesity - induced hypertension, Hypertension, 19, pp. I61-I66, (1992)
[7]  
Defronzo R.A., The effect of insulin on renal sodium metabolism, Diabetologia, 21, pp. 165-171, (1981)
[8]  
Levinson P.D., Iosiphidis A.H., Gann D.S., Hormone and cathecolamine responses accompanying the antinatriur- esis of glucose ingestion, Am J Hypertens, 2, (1989)
[9]  
Reaven G.M., Ho H., Hoffmann B.B., Somatostatin inhibition of fructose-induced hypertension, Hypertension, 14, pp. 117-120, (1989)
[10]  
Carretta R., Fabris B., Fischetti F., Et al., Reduction of blood pressure in obese hyperinsulinaemic hypertensive patients during somatostatin infusion, J Hypertens, 7, pp. S196-S197, (1989)