Insulin resistance has been implicated in the pathogenesis of
essential hypertension. Studies from other countries discovered
insulin resistance; in people with
essential hypertension in was also associated with
obesity, however,
insulin resistance was found in lean people too. In
obesity,
insulin resistance occurs secondarily to many physiopathological states and circulating factors which adversely affects
insulin action. The metabolic abnormality in this action was mainly found in relation to abdominal fat; in other cases,
insulin resistance was found to be inherited. Hyperinsulinaemia can actually increase blood pressure and is associated with venous and arterial
thrombosis and it also rises
lipid levels. It is interesting too that
insulin resistance and hyperinsulinaemia are associated with impaired fibrinolysis through high levels of
fibrinogen and
plasminogen activator inhibitor of endothelial type and in identifying individuals prone to
myocardial infarction. Some
antihypertensive drugs like beta-blockers, methyl-
dopa and
diuretics increase
insulin resistance, while
angiotensin converting enzyme-inhibitors have not shown any adverse metabolic affects. Alfa-1-blocker were beneficial and alfa-2-agonists were neutral, whereas
calcium channel-antagonists are still in controversy. Treatment should be designed to improve the metabolic state; physical exercise, a diet rich in fruit, vegetable and rott vegetables, the reduction of abdominal fat and, finally, the use of
antihypertensive drugs which decrease
insulin resistance would be expected to reverse hyperinsulinaemia.
Biguanides like
metformin have also been found to reduce
insulin resistance.