Pressure-volume regulation in hypertension

Abstract

In all forms of hypertension, including human essential hypertension, pressure natriuresis is abnormal because sodium excretion is the same as in normotension despite increased arterial pressure. Considerable evidence indicates that this resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as an adaptation to increased blood pressure. Because human essential hypertension is a heterogeneous disease, it is likely that multiple neurohumoral and intrarenal defects contribute to abnormal pressure natriuresis and increased blood pressure. Physiological studies have shown that renal abnormalities that cause increased distal and collecting tubule reabsorption, decreased glomerular filtration coefficient or loss of nephrons also cause decreased slope of pressure natriuresis (salt-sensitive hypertension), whereas increased preglomerular resistance causes a parallel shift of pressure natriuresis (salt-insensitive hypertension). Comparison of the characteristics of pressure natriuresis (such as salt-sensitivity of blood pressure) in hypertensive subjects with those forms of experimental hypertension of known origin can provide insight into the etiology of human hypertension. With long-standing hypertension, pathological changes in the glomeruli and renal arterioles may further shift pressure natriuresis and exacerbate hypertension.