Multifactorial insulin resistance and clinical impact in hypertension and cardiovascular diseases.
Insulin resistance and hyperinsulinemia have been observed in over 70% of the nonobese, nondiabetic subjects with essential hypertension (HT). Alpha-1 blockers, ACE-antagonists, long-acting Ca blockers including nifedipine CR, some form of beta-blockers, tilisolor, which is reported to increase blood flow, improve insulin sensitivity when blood pressure is better controlled. Decrease of serum potassium during insulin sensitivity test and intraplatelet free Ca2+ concentration is positively and negatively correlated with insulin sensitivity, respectively. Blood pressure is correlated with insulin resistance, which is also observed in secondary HT. The resistance is correlated with salt sensitivity as well as impaired nocturnal fall of blood pressure. These suggest the possible association of insulin resistance with altered intracellular cation metabolism. Insulin resistance and associated hyperinsulinemia have been observed in effort as well as vasospastic angina pectoris (VSAP), atherothrombotic cerebral infarction, and in ASO without obesity, HT, or diabetes, suggesting the resistance resulting from endothelial dysfunction. Insulin resistance has been observed in heart failure and is correlated with angiotensin II. Resistance is also observed in hypertrophic cardiomyopathy and is partially correlated with TNF-alpha. These results indicate that insulin resistance seem to be multifactorial. An effort to normalize insulin sensitivity is crucial to eliminate multiple risk factors as well as to prevent the progression of atherosclerotic vascular lesions.
Harano
Yutaka
Y
Koshien University College of Nutrition, 10-1, Momijigaoka, Hyogo, Takarazuka, Japan.
Suzuki
Masaaki
M
Koyama
Yuko
Y
Kanda
Munetake
M
Yasuda
Satoshi
S
Suzuki
Kazutaka
K
Takamizawa
Itaru
I
D000959:Antihypertensive Agents / Q000145:classification / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D008954:Models, Biological
D000959:Antihypertensive Agents