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Obesity and Hypertension: Roles of Hyperinsulinemia, Sympathetic Nervous System and Intrarenal Mechanisms^1,2,

The University of Mississippi Medical Center, Jackson, MS 39216-4505

Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remain to be determined.

KEY WORDS: • obesity • hypertension • sympathetic nervous system • insulin • kidney

¹ Presented as part of the symposium "Insulin Resistance, Obesity and Hypertension" given at the Experimental Biology '94 meeting, Anaheim, CA, on April 27, 1994. This symposium was sponsored by the American Institute of Nutrition. Guest editor for this symposium was Michael B. Zemel, The University of Tennessee, Knoxville, TN.

² Supported by NIH grants HL23502, HL39399 and HL51971.

³ To whom correspondence should be addressed: Department of Physiology and Biophysics, The University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505.

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