ABSTRACT
The endogenous release of nitric oxide (NO) contributes to the maintenance of blood pressure and this, in turn, is a stimulus for NO production. The role of NO in hypertension is very controversial. Recent research work is showing the existence of profound differences in the role of NO depending on the model of hypertension. In genetic and renovascular hypertension, the production of NO is increased probably as a compensatory mechanism against the overproduction of different vasoconstrictors. In genetic hypertension, however, the bioactivity of NO is diminished. In salt-sensitive hypertension, NO production is impaired probably due to a deficiency of the substrate for NO synthase. In human essential hypertension, pharmacological experiments reveal an impaired NO dilator mechanism.
