Neuroendocrinal basis of essential hypertension, and its management

Neuroendocrinal basis of essential hypertension, and its management

There are basically two mechanisms for development of hypertension. First, is due to salt and water retention, which is mostly responsible for diastolic hypertension, and works through the HPA axes and via the renin angiotensin (RAA) pathway, and glucocorticoid and mineralocorticoid secretion is responsible for it. Hypertension in younger patients, associated with tachycardia, metabolic syndrome, and pregnancy induced hypertension (including preeclampsia) are examples of this mechanism. Drugs which act on HPA axes and RAA pathway, such as ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, diuretics, metformin are useful in managing such cases.

The second mechanism is due to alpha adrenergic induced vasoconstriction, and change in collagen elastin ratio of the blood vessels. With ageing, excessive alpha adrenergic stimulation causes elastin degradation and collagen deposition leading to stiffer blood vessels. This presents as isolated systolic hypertension. Diastolic hypertension might also be present if there is both alpha and beta adrenergic stimulation. It is also associated with chronic inflammatory illnesses such as rheumatoid arthritis. Drug of choice for managing this is calcium channel blockers like amlodepine, cilnidepine, central sympatholytics such as clonidine, and renal denervation.

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