INSULIN-MEDIATED VASODILATION - IMPAIRMENT WITH INCREASED BLOOD-PRESSURE AND BODY-MASS

被引:133
作者
FELDMAN, RD
BIERBRIER, GS
机构
[1] UNIV WESTERN ONTARIO,DEPT MED,LONDON N6A 3K7,ONTARIO,CANADA
[2] UNIV WESTERN ONTARIO,DEPT PHARMACOL & TOXICOL,LONDON N6A 3K7,ONTARIO,CANADA
关键词
D O I
10.1016/0140-6736(93)91708-T
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Insulin resistance is associated with hypertension although it is not known if this relationship is casual. Studies have shown that insulin increases skeletal-muscle blood flow despite also increasing sympathetic activity. To determine whether insulin may act as a direct vasodilator and whether insulin-mediated vascular effects are altered in hypertension, we studied insulin-mediated alterations in dorsal-hand-vein compliance in normotensive and mild and borderline hypertensive subjects. In phenylephrine pre-constricted vessels, insulin caused a dose-dependent increase in venous distensibility. Insulin-mediated venodilation was significantly impaired in hypertensive subjects. The vasodilator potency of insulin was significantly correlated with both blood pressure and body mass index. Insulin may be an endogenous vasodilator. Further, in hypertensive and obese subjects, impairment of insulin-mediated vasodilation may contribute to the increase in peripheral resistance characteristic of hypertension.
引用
收藏
页码:707 / 709
页数:3
相关论文
共 22 条
[1]   A NEW TECHNIQUE FOR RECORDING COMPLIANCE OF HUMAN HAND VEINS [J].
AELLIG, WH .
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 1981, 11 (03) :237-243
[2]   THE VASODILATOR ACTION OF INSULIN - IMPLICATIONS FOR THE INSULIN HYPOTHESIS OF HYPERTENSION [J].
ANDERSON, EA ;
MARK, AL .
HYPERTENSION, 1993, 21 (02) :136-141
[3]   INSULIN INCREASES SYMPATHETIC ACTIVITY BUT NOT BLOOD-PRESSURE IN BORDERLINE HYPERTENSIVE HUMANS [J].
ANDERSON, EA ;
BALON, TW ;
HOFFMAN, RP ;
SINKEY, CA ;
MARK, AL .
HYPERTENSION, 1992, 19 (06) :621-627
[4]   HYPERINSULINEMIA PRODUCES BOTH SYMPATHETIC NEURAL ACTIVATION AND VASODILATION IN NORMAL HUMANS [J].
ANDERSON, EA ;
HOFFMAN, RP ;
BALON, TW ;
SINKEY, CA ;
MARK, AL .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (06) :2246-2252
[5]   SKELETAL-MUSCLE IS A PRIMARY SITE OF INSULIN RESISTANCE IN ESSENTIAL-HYPERTENSION [J].
CAPALDO, B ;
LEMBO, G ;
NAPOLI, R ;
RENDINA, V ;
ALBANO, G ;
SACCA, L ;
TRIMARCO, B .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1991, 40 (12) :1320-1322
[6]  
CREAGER MA, 1985, J PHARMACOL EXP THER, V235, P709
[7]   A LOW-SODIUM DIET CORRECTS THE DEFECT IN BETA-ADRENERGIC RESPONSE IN OLDER SUBJECTS [J].
FELDMAN, RD .
CIRCULATION, 1992, 85 (02) :612-618
[8]   LOW SODIUM DIET CORRECTS THE DEFECT IN LYMPHOCYTE BETA-ADRENERGIC RESPONSIVENESS IN HYPERTENSIVE SUBJECTS [J].
FELDMAN, RD ;
LAWTON, WJ ;
MCARDLE, WL .
JOURNAL OF CLINICAL INVESTIGATION, 1987, 79 (01) :290-294
[9]   DEFECTIVE VENOUS BETA-ADRENERGIC RESPONSE IN BORDERLINE HYPERTENSIVE SUBJECTS IS CORRECTED BY A LOW SODIUM DIET [J].
FELDMAN, RD .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (03) :647-652
[10]   ESSENTIAL-HYPERTENSION, METABOLIC DISORDERS, AND INSULIN RESISTANCE [J].
FERRANNINI, E ;
NATALI, A .
AMERICAN HEART JOURNAL, 1991, 121 (04) :1274-1282