Diabetes mellitus and hypertension each confer increased cardiovascula
r risk. That risk is much greater when the diseases coexist and is fur
ther magnified by their frequent association with dyslipidemia and cen
tral obesity. Insulin resistance appears to be an important common com
ponent to these four entities, whether or not the relationship is trul
y cause and effect. Increased renal tubule absorption of sodium and in
creased sympathetic nervous system stimulation from insulin have been
said to be the mechanisms by which elevated levels of insulin cause hy
pertension. However, animal experiments suggest that these are short-t
erm effects only and that long-term insulin may actually increase peri
pheral blood flow and reduce blood pressure. Experiments in humans sug
gest that the insulin resistant state in obese patients and type II di
abetics is associated with a decrease of the usual vasodilatory effect
of insulin. Antihypertensive drugs have differing effects on insulin
resistance. Angiotensin converting enzyme inhibitors, alpha-adrenergic
blockers, and dihydropyridines appear to improve insulin sensitivity.
Other calcium channel blockers appear to be neutral, as is furosemide
. Thiazide diuretics, spironolactone, and beta-adrenergic blockers imp
air insulin sensitivity. The drugs that increase insulin sensitivity a
lso tend to improve dyslipidemia or remain lipid neutral. In contrast,
those drugs that tend to impair insulin sensitivity also tend to wors
en dyslipidemia.