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Nitric oxide (NO) pathway is involved in various physiological and pathophysiological processes. NO is synthesised by NO synthase. Three isoforms, ecNOS, nNOS, iNOS have been identified to date, that are encoded by 3 distinct genes on chromosome 7, 12 and 17 respectively. L-arginine is likely involved in the control of NO synthesis. In the kidney, NO regulates glomerular hemodynamics by modulating the ultrafiltration coefficient and afferent and efferent renal arteriolar resistance. NO is further involved in the pressure-natriuresis mechanism and in the tubuloglomerular feedback. Several physiopathological models have underlined the importance of the NO in arterial hypertension and in glomerular inflammation.

The mechanisms involved in the physiology of pregnancy and in the pathophysiology of preeclampsia are still largely unknown. Prostaglandins metabolism, especially an imbalance between thromboxane A2 and prostacyclin does not appear sufficient to explain all the observed changes. Recent studies have shown that nitric oxide (NO), a vasodilating and a platelet anti-aggregating factor, could play a pivotal role in inducing hemodynamic changes during pregnancy. NO is produced in excess during pregnancy, mainly in uterine and renal vascular beds. Similarly, NO is in part responsible for the non-responsiveness of the vessels to vasoactive agents and plays a relevant role in peripheral vasodilation and in lowering systemic blood pressure. Furthermore, NO improves blood supply to the fetal-placental unit and to maternal kidneys. An impaired NO metabolism in pregnant rats induces changes similar to those observed in human preeclampsia. NO pathway represents a new approach to the physiology of pregnancy and to the pathophysiology of preeclampsia. Moreover, NO donors might be carefully proposed as new therapeutic agents in this disorder.