Atrial natriuretic peptide influence on nitric oxide system in kidney and heart.

Atrial natriuretic peptide (ANP) and nitric oxide (NO) induce diuresis, natriuresis and diminish vascular tone. Our previous studies showed NO system is involved in ANP hypotensive effect. The aim was to investigate ANP effects on renal and cardiac NO-synthase (NOS) activity. Rats were divided into two groups: group I, infused with saline (1 h, 0.05 ml/min); group II, received ANP bolus (5 microg/kg)+ANP infusion (1 h, 0.2 microg/kg x min). NADPH-diaphorase activity (NADPH-d) was determined in kidney and heart. NOS catalytic activity was determined in renal medulla and cortex and cardiac atria and ventricle by measuring the conversion of l-[U(14)C]-arginine to l-[U(14)C]-citrulline. In group I, NOS activity was determined in basal conditions and plus 1 microM ANP and in group II, NOS activity was determined in basal conditions. NADPH-d was higher in group II than in group I in glomeruli, proximal tubule, cortical and medullar collecting duct, right atria and left ventricle. NOS activity was increased by in vitro ANP addition and, in vivo, ANP infusion in all the studied tissues. ANP treatment increases renal and cardiac NO synthesis. This effect would be independent on the hemodynamic changes induced by ANP. The activation of NO pathway would be one of the mechanisms involved in diuretic, natriuretic and hypotensive effects of ANP.

Renal and vascular nitric oxide system in reduced renal mass saline hypertension.

BACKGROUND: Reduction in renal mass is associated with several structural and functional adaptations including compensatory renal growth and hemodynamic changes. The mediators of the renal hemodynamic adaptations have not been definitively identified. Several investigators have postulated that nitric oxide (NO) is involved this physiological mechanisms. The purpose of this study was to evaluate the role of vascular and renal NO pathway in the model of subtotal nephrectomy-salt load hypertension. MATERIALS AND METHODS: Wistar rats with 75% renal mass reduction (RMR) and saline load were studied during 4 weeks. Weekly, indirect systolic blood pressure (SBP) were measured. One week after nephrectomy, animals were divided in two groups, hypertensive (SBP > 140 mm Hg) and normotensive (SBP < 140 mm Hg). Urinary excretion of nitrates and nitrites (NOx), urinary chemioluminiscence levels and NOS activity in the left kidney and in the thoracic aorta artery were determined at the fourth week after subtotal nephrectomy. RESULTS: Urinary excretion of sodium was higher in normotensive rats than hypertensive rats and in both groups this parameter was higher than in sham rats. NOx excretion and NOS activity in the different nephron segments were higher in normotensive rats than in the hypertensive ones. In contrast, NOS activity in aorta sections and urinary chemiluminescence levels in hypertensive animals were enhanced compared with normotensive rats. These parameters were higher in both groups of nephrectomized rats than in sham ones. CONCLUSION: This study provides evidence to support the fact that the activation of the renal NO system is an important mechanism whereby the remnant kidney regulates sodium and water balance, contributing to control the arterial blood pressure in the renal mass reduction and saline load model.