Abstract
Human essential hypertension is due to interacting genetic and environmental factors. Spontaneously hypertensive rats have been genetically selected as models in this setting. The genetically hypertensive rat model that we have selected is the only one to associate mild hypertension with a "metabolic syndrome" (increased body weight, proteinuria and hyperlipidemia and elevated insulin/glucose ratio). This is a renin-dependent model of hypertension, in which low-dose (non antihypertensive) angiotensin-converting-enzyme inhibitor therapy affords significant and durable nephroprotection.
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