Abstract:

Obesity is linked with the growth of white adipose tissue and associated chronic hyperleptinemia. Leptin is a hormone-like cytokine or adipokine secreted mainly from adipose tissue. High leptin state in obesity rapidly causes selective resistance, focused in the arcuate nucleus of the hypothalamus, and centered round leptin’s role in food intake and satiety. This resistance lowers the body’s reaction to food intake and prevents the anorexigenic effects of leptin. As this resistance builds up, the intake of food increases causing an enhancement in body adiposity and leptin levels. However, some pathways do not build resistance to leptin and continue to exhibit the stimulatory effects, which cause a persistent stimulation of sympathetic nervous system (SNS), particularly in the kidneys and skeletal muscles. The increase in SNS activity in the kidney, along with the endothelial dysfunction and oxidative stress, lead to an increase in blood pressure. Apart from leptin's effects on SNS and renal function, this adipokine influences vascular health and hypertension through several phenomena or mechanisms such as baroreflex sensitivity, release of nitric oxide and cardiac hormones. In this review, an attempt has been made to highlight different aspects of leptin biology, which are relevant to hypertension.

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