INSULIN-RESISTANCE AND MYOCARDIAL HYPERTROPHY IN THE ATTENUATED REDUCTION IN MEAN ARTERIAL-PRESSURE AFTER A GLUCOSE-LOAD IN HYPERTENSIVE PATIENTS

Citation
Ml. Souza et al., INSULIN-RESISTANCE AND MYOCARDIAL HYPERTROPHY IN THE ATTENUATED REDUCTION IN MEAN ARTERIAL-PRESSURE AFTER A GLUCOSE-LOAD IN HYPERTENSIVE PATIENTS, Brazilian journal of medical and biological research, 28(9), 1995, pp. 967-972
Citations number
17
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
0100879X
Volume
28
Issue
9
Year of publication
1995
Pages
967 - 972
Database
ISI
SICI code
0100-879X(1995)28:9<967:IAMHIT>2.0.ZU;2-6
Abstract
Although long recognized, the vasodilator effect of insulin has been r elatively neglected over the last few pears. Recent reports have focus ed on the sympathetic and antinatriuretic actions of this hormone. In the first part of the present study we characterized the reduction in blood pressure after a glucose load in hypertensive patients with and without insulin resistance. Fourteen hypertensive Caucasian patients a nd ten Caucasian controls were submitted to a standard oral glucose to lerance test (OGTT) and intravenous insulin tolerance test (15-min ITT ). In the hypertensive patients with insulin resistance the reduction in mean arterial pressure (MAP) after a glucose load was blunted (6.7 +/- 1.7% (N = 5)) when compared to insulin-sensitive (12.9 +/- 1.1% (N = 9)) and normal subjects (10.1 +/- 0.8%). In the second part of the study we investigated whether hypertensive patients with myocardial hy pertrophy were more insulin resistant than hypertensive individuals wi th a normal cardiac mass. The glucose disappearance rate (Kitt) was lo wer in hypertensive patients with myocardial hypertrophy (6.0 +/- 1.0 (N = 6)) when compared to hypertensive patients without myocardial hyp ertrophy (8.2 +/- 1.0%/min (N = 8)); suggesting an association between this organomegaly and insulin resistance. In conclusion, our results suggested that 1) insulin resistance: rather than hyperinsulinemia, ac ts as a risk factor for the development of hypertension, because of in sulin's inability to decrease MAP in this situation, and 2) there is a n association between left ventricular hypertrophy and insulin resista nce in hypertensive patients.