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The Physiology and Pharmacology of Hypertension

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To establish long-term determination of blood pressure, research was carried out in the families that have historically high or severely low pressure and it was identified that the mutations in many steps of the above-mentioned pathway are the main cause. Mutations increase renal salt reabsorption raises blood pressure and those that diminish salt reabsorption lower blood pressure. The pathophysiologic link between salt and blood pressure can be known form the relationship between salt and vascular volume homeostasis. The increased net renal salt reabsorption leads to increase in water reabsorption in order to maintain sodium concentration at or near 140mM.

This results in increased intravascular volume augment venous blood return to the heart, thus increasing the cardiac output and finally leading to elevated blood pressure. In the opposite end, if there is an impaired reabsorption of salt will lead to decrease in blood volume and blood pressure. The Pathophysiologic characteristics of Hypertension: There is no established known cause of the pathophysiological condition of hypertension. The diastolic pressure repeatedly is more than 90 mm Hg and the total peripheral resistance is usually increased. The pulse pressure possibly increases or decreases.

The Cardiac output is normal or elevated in the early stages of the disease. The cardiac work is also elevated. There is altered renal physiology with accelerated natriuresis and reduced renal flow. In hypertension, the normal blood flows to most of the regions of the human body. But there is diminished renal and skin blood flow and increased muscle flow may develop. In addition to that, the Plasma volume may be inversely related to diastolic pressure. Further, there is hyper-reactivity of pressure to stress, abnormal vascular reactivity, and impaired homeostasis.

(Vikrant S, 2001)Drugs of different classes are used to control hypertension, either alone or in combination.

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