Deficient production of nitric oxide induces volume-dependent hypertension

To study the influence of nitric oxide on renal function.

Nitric oxide synthesis was inhibited and the effects on renal parameters were determined.

Nitric oxide synthesis was progressively blocked by the intravenous administration of increasing doses of NG-nitro-arginine methylester (L-NAME) and then (c)GMP was administered.

The blockade of nitric oxide synthesis first induced a marked fall in urinary sodium excretion, and later, a sustained increase in mean arterial pressure. These effects were reversed by 8-bromide cGMP. Nitric oxide-dependent cGMP formation was higher in the inner medulla than in any other part of the renal parenchyma, and the inhibition of nitric oxide synthesis significantly decreased both pressure- and volume expansion-induced natriuresis.

Both the natriuretic and vasodilator tone maintained by nitric oxide are ultimately due to the production of cGMP. Nitric oxide-induced formation of cGMP appears to be the major factor that links changes in renal medullary circulation to those of sodium excretion. Sufficient inhibition of nitric oxide synthesis to decrease sodium excretion without altering blood pressure induces volume-dependent hypertension because blood pressure is elevated by an increased sodium intake.