Journal
MEDICAL CLINICS OF NORTH AMERICA
Volume 88, Issue 1, Pages 63-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/S0025-7125(03)00128-7
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL066119] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL066119-04] Funding Source: Medline
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Insulin (INS) resistance use is an integral component of the cardio-metabolic syndrome, which often progresses to type 2 diabetes and cardiovascular disease (CVD) events. Hyperinsulinemia, an important component of the cardiometabolic syndrome, may predispose to the development of hypertension, another important part of this syndrome. Hyperinsulinemia may directly contribute to elevated blood pressure by enhancing sympathetic nervous system activity and promoting renal sodium retention. INS may also indirectly increase blood pressure by decreasing the signaling processes that are important for vascular relaxation. Further, an overexpression of the tissue renin-angiotensin system seems to contribute to impaired INS use in skeletal muscle and fat tissue and diminished vasorelaxation. Therapeutic strategies that improve INS sensitivity may impede the progression of impaired INS sensitivity to that of clinical diabetes, and reduce blood pressure, renal disease progression, and CVD events.
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