The experimental model of chronic inhibition of
nitric oxide (NO) production has proven to be a useful tool to study cardiovascular and renal lesions produced by this type of
hypertension, which are similar to those found in human
hypertension. It also offers a unique opportunity to study the interaction of NO with the humoral systems, known to have a role in the normal physiology of vascular tone and renal function. This review provides a thorough and updated analysis of the interactions of NO with the endocrine system. There is special focus on the main vasoactive factors, including the renin-angiotensin-aldosterone system,
catecholamines,
vasopressin, and
endothelin among others. Recent discoveries of crosstalk between the endocrine system and NO are also reported. Study of these humoral interactions indicates that NO is a molecule with ubiquitous function and that its inhibition alters virtually to all other known regulatory systems. Thus,
hypothyroidism attenuates the pressor effect of NO inhibitor N-nitro-
L-arginine methyl ester, whereas
hyperthyroidism aggravates the effects of NO synthesis inhibition; the
sex hormone environment determines the blood pressure response to NO blockade; NO may play a homeostatic role against the prohypertensive effects of
mineralocorticoids,
thyroid hormones and
insulin; and finally, NO deficiency affects not only blood pressure but also
glucose and
lipid homeostasis, mimicking the human
metabolic syndrome X, suggesting that NO deficiency may be a link between metabolic and
cardiovascular disease.