Objective: Nitric oxide is an important modulator of vascular tone but also of the sodium and water balance. These phenomena appear to be of particular relevance in the control of blood pressure and the development of arterial hypertension. Design and method: We evaluated in 4 week-old Wistar Kyoto normotensive rats the effects of chronic inhibition of nitric oxide synthase through NG-nitro-L-arginine methyl ester (L-NAME, 7.5 mg / kg / day per 4 weeks) on water and sodium balance. Results: The dose of L-NAME administered orally for 4 weeks did not generate a significant increase in blood pressure (116 ± 10 vs 112 ± 8). The volume of diuresis was reduced, associated with an increase in urine osmolarity in the group treated with L-NAME. Natriuresis levels were not significantly different between L-NAME treated and untreated rats. Urinary aquaporin2/creatinine ratio was significantly elevated in L-NAME group of rat (p < 0.05). Plasma and urinary metabolites of nitric oxide (NOx) were reduced in L-NAME treated rats as compared to untreated. Conclusions: These results support that nitric oxide synthase inhibition, at subpressor doses, determine a positive water balance by increasing tubular effect of vasopressin that lead to higher tubular water channel (aquaporin2) expression, and subsequently to the shedding in the urine.
CHRONIC NITRIC OXIDE SYNTHASE INHIBITION INCREASES RENAL VASOPRESSIN EFFECTS IN NORMOTENSIVE RAT
Bergamaschi, E.;
2019-01-01
Abstract
Objective: Nitric oxide is an important modulator of vascular tone but also of the sodium and water balance. These phenomena appear to be of particular relevance in the control of blood pressure and the development of arterial hypertension. Design and method: We evaluated in 4 week-old Wistar Kyoto normotensive rats the effects of chronic inhibition of nitric oxide synthase through NG-nitro-L-arginine methyl ester (L-NAME, 7.5 mg / kg / day per 4 weeks) on water and sodium balance. Results: The dose of L-NAME administered orally for 4 weeks did not generate a significant increase in blood pressure (116 ± 10 vs 112 ± 8). The volume of diuresis was reduced, associated with an increase in urine osmolarity in the group treated with L-NAME. Natriuresis levels were not significantly different between L-NAME treated and untreated rats. Urinary aquaporin2/creatinine ratio was significantly elevated in L-NAME group of rat (p < 0.05). Plasma and urinary metabolites of nitric oxide (NOx) were reduced in L-NAME treated rats as compared to untreated. Conclusions: These results support that nitric oxide synthase inhibition, at subpressor doses, determine a positive water balance by increasing tubular effect of vasopressin that lead to higher tubular water channel (aquaporin2) expression, and subsequently to the shedding in the urine.
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