Resistance to metabolic actions of insulin and its role in hypertension

Richard L. Summers, Michael W Brands, Henry Keen, Magdalena Alonso-Galicia

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Insulin resistance and hyperinsulinemia have been postulated to be important in raising blood pressure in obese as well as lean hypertensive individuals. However, cause-and-effect relationships among these variables have not been clearly established. The three most widely used methods to assess insulin resistance in vivo (fasting plasma insulin, glucose disposal after a glucose load, or glucose disposal during a hyperinsulinemic euglycemic clamp) may provide different estimates of insulin resistance under various physiological and pathophysiological conditions. Fasting hyperinsulinemia may reflect mainly hepatic insulin resistance, whereas impairment of glucose disposal indicates resistance to the metabolic effects of insulin in skeletal muscle. The importance of these different sites of insulin resistance in the etiology of cardiovascular diseases, however, is still unclear. Although hyperinsulinemia and insulin resistance have been speculated to cause hypertension, most of the evidence supporting this hypothesis has come either from correlation studies or from short-term studies of the cardiovascular, renal, and sympathetic effects of insulin. The few long-term studies that have been conducted in dogs and in humans do not support the insulin concept of hypertension. In fact, these studies suggest that the vasodilator actions of insulin tend to reduce, rather than elevate, blood pressure. Correlations between insulin resistance, hyperinsulinemia, and hypertension do not appear to be explainable by the concept that insulin resistance occurs secondary to hypertension. Obesity may be a key factor in explaining these relationships; weight gain appears to cause insulin resistance, compensatory hyperinsulinemia, and hypertension through parallel, but not necessarily linked, mechanisms. However, insulin resistance and compensatory hyperinsulinemia may contribute to increased risk of other cardiovascular diseases associated with hypertension, such as coronary artery disease. Am J Hypertens 1994;7:772–788.

Original languageEnglish (US)
Pages (from-to)772-788
Number of pages17
JournalAmerican journal of hypertension
Volume7
Issue number8
DOIs
StatePublished - Jan 1 1994

Fingerprint

Insulin Resistance
Insulin
Hypertension
Hyperinsulinism
Glucose
Fasting
Cardiovascular Diseases
Blood Pressure
Glucose Clamp Technique
Vasodilator Agents
Weight Gain
Coronary Artery Disease
Skeletal Muscle
Obesity
Dogs
Kidney
Liver

Keywords

  • Blood flow
  • Glucose intolerance
  • Insulin resistance
  • Liver
  • Skeletal muscle

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Resistance to metabolic actions of insulin and its role in hypertension. / Summers, Richard L.; Brands, Michael W; Keen, Henry; Alonso-Galicia, Magdalena.

In: American journal of hypertension, Vol. 7, No. 8, 01.01.1994, p. 772-788.

Research output: Contribution to journalArticle

Summers, Richard L. ; Brands, Michael W ; Keen, Henry ; Alonso-Galicia, Magdalena. / Resistance to metabolic actions of insulin and its role in hypertension. In: American journal of hypertension. 1994 ; Vol. 7, No. 8. pp. 772-788.
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