Role of the Kidneys in the Regulation of Intra-and Extra-Renal Blood Pressure

Abstract

Hypertension is one of the most common chronic diseases of human, affecting more than one billion people worldwide. When it becomes chronic, hypertension leaves behind cardiac hypertrophy, heart failure, stroke, and kidney disease, resulting in substantial morbidity and mortality. Treatments that effectively reduce blood pressure can prevent these complications. Abnormalities in the production of urine by the kidneys have been implicated in increased vascular resistance, leading to high blood pressure and increased cardiac mass. By matching urinary excretion of salt and water with dietary intake, balance is usually attained, thereby maintaining a constant extracellular fluid volume and blood pressure. Based on the capacity for the kidney to excrete sodium, this blood pressure-altering mechanism should have sufficient advantage to limit intravascular volume and consequently lower blood pressure in response to a range of stimuli from elevated heart rate to increase peripheral vascular resistance. A major determinant of the level of intra- and extra- renal blood pressure is therefore sodium handling, and it is controlled by complex physiological mechanism by hormones, inflammatory mediators, and the sympathetic nervous system. Homoeostasis and favourable influence sodium balance are a basic mechanism of efficacy for diuretics and dietary sodium restriction in hypertension. Renin Angiotensin System (RAS) inhibitors, vasodilators, and β-blockers work to facilitate pressure-natriuresis. Also, WNK signaling pathways, soluble inflammatory mediators, and pathways regulating extra-renal sodium disposition may be the focus towards elimination of sodium and reducing blood pressure in hypertension.