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Obesity rates have surged to pandemic levels, placing tremendous burden on our society. This chronic and complex disease is related to the development of many life-threatening illnesses including cardiovascular diseases. Hypertension caused by obesity increases the risk for cardiovascular mortality and morbidity by promoting stroke, myocardial infarction, congestive heart failure, and end-stage renal disease. Overwhelming evidence supports neural origins for obesity-induced hypertension and pinpoints the adipose-derived hormone, leptin, and the sympathetic nervous system as major causal factors. Hyperleptinemia in obesity is associated with selective leptin resistance where leptin's renal sympathoexcitatory and pressor effects are preserved while the metabolic actions are impaired. Understanding the mechanisms driving this phenomenon is critical for developing effective therapeutics. This review describes the neural mechanisms of obesity-induced hypertension with a focus on the molecular and neuronal substrates of leptin action.
Laule et al. (Mon,) studied this question.