O'Hare J A
Joslin Diabetes Center, New England Deaconess Hospital, Harvard Medical School, Boston, Massachusetts.
Am J Med. 1988 Mar;84(3 Pt 1):505-10. doi: 10.1016/0002-9343(88)90273-2.
The epidemiologic link between obesity and hypertension is more clearly emerging to be one between insulin resistance and hypertension. Relative insulin resistance occurs not only in obese hypertensive patients but also in non-obese lean essential hypertensive patients. Although insulin has complex actions on the circulation, plausible mechanisms by which insulin might raise blood pressure include renal sodium retention and stimulation of the sympathetic nervous system. However, the evidence that insulin can actually raise blood pressure in the long-term is lacking. Since hypertension does not develop in all obese or insulin-resistant subjects, the relationship must be modulated by other genetic or environmental factors. Obesity, diminished physical conditioning, aging, and diabetes are ubiquitous contributors to relative insulin resistance and all are associated with a tendency for blood pressure to rise. Conditions and agents associated with acquired insulin resistance and secondary forms of hypertension include pregnancy, oral contraceptives, acromegaly, and glucocorticoids. Although type 2 non-insulin-dependent diabetes is a state of increased insulin resistance, hypertension is partly sustained by secondary renal mechanisms. Future research should identify the genetic and environmental determinants of insulin resistance in hypertension and utilize these in therapy.
