Abnormal pressure-natriuresis in hypertension: role of nitric oxide

The kidneys have a critical role in long-term control of arterial pressure by regulating extracellular fluid and plasma volume. According to the renal body fluid feedback mechanism for long-term control, persistent hypertensi on can only occur as a result of a reduction in renal sodium excretory func tion or a hypertensive shift in the pressure-natriuresis relationship. Alth ough an abnormal relationship between renal perfusion pressure and renal so dium excretion has been identified in every type of hypertension where it h as been sought, factors responsible for this effect are still unclear. Nitr ic oxide (NO) is produced within the kidney and plays an important role in the control of many intrarenal processes which regulate the renal response to changes in perfusion pressure and thus, help determine plasma volume and blood pressure. Numerous studies have shown that long-term inhibition of N O synthesis results in a chronic rightward shift and marked attenuation in renal pressure-natriuresis. Recent studies have shown that certain animal m odels of genetic hypertension and forms of human hypertension areas are ass ociated with a decrease in NO synthesis. Reductions in NO synthesis reduces renal sodium excretory function not only through direct actions on the ren al vasculature, but through modulation of other vasoconstrictor processes a nd through direct and indirect alterations in tubular sodium transport. The causes and consequences of the dysregulation of NO in hypertension and oth er renal disease processes remain an important area of investigation.