IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
artículos
Título:
Chronic treatment with C-type natriuretic peptide impacts differently in the aorta of normotensive and hypertensive rats
Autor/es:
CANIFFI C; TOMAT A; ARRANZ C; SUEIRO L; TOBLLI JE ; CERNIELO M; GONZALEZ MAGLIO DANIEL
Revista:
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Editorial:
SPRINGER
Referencias:
Lugar: Berlin; Año: 2019 p. 1103 - 1115
ISSN:
0031-6768
Resumen:
The aim of this study was to determine whether exogenous administration ofC-typenatriuretic peptide (CNP) induces functional and morphologicalvascularchanges in spontaneously hypertensive rats (SHR) compared withnormotensiverats. Male 12-week-old normotensive Wistar and SHR wereadministeredwith saline (NaCl 0.9%) or CNP (0.75 ìg/h/100 g) for 14 days(subcutaneousmicro-osmotic pumps). Systolic blood pressure (SBP) wasmeasuredin awake animals and renal parameters were evaluated. Afterdecapitation,the aorta was removed, and vascular morphology, profibroticmarkers,and vascular reactivity were measured. In addition, nitric oxide (NO)systemand oxidative stress were evaluated. After 14-days of treatment, CNPeffectivelyreduced SBP in SHR without changes in renal function. CNPattenuatedvascular remodeling in hypertensive rats, diminishing bothprofibroticand pro-inflammatory cytokines. Also, CNP activated the vascularNOsystem and exerted an antioxidant effect in aortic tissue of both groups,diminishingsuperoxide production and thiobarbituric acid-reactivesubstances,and increasing glutathione content. These results show thatchronictreatment with CNP attenuates the vascular damage development in amodelof essential hypertension, inducing changes in fibrotic, inflammatory,oxidative,and NO pathways that could contribute to beneficial long-termeffectson vascular morphology, extracellular matrix composition, and function. Theknowledge of these effects of CNP could lead to improved therapeutic strategiesto not only control BP but also reduce vascular damage, primarily responsiblefor the risk of cardiovascular events.