Nitric oxide bioavailability is also regulated by the CGMP pathway in L‐NAME hypertensive cardiomyopathy of rats View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-02

AUTHORS

S. Ferreira‐Melo, J. C. Yugar‐Toledo, W. A. Souza, A. J. Thomaz, K. G. Franchini, O. R. Coelho, I. Lucca, H. Moreno

ABSTRACT

Cardiac hypertrophy and large areas of perivascular and myocardial fibrosis characterize the hypertensive cardiomyopathy induced by NO biosynthesis inhibition (HC-NOI) in rats. However, the pathophysiology of these alterations is still not fully clear. For example, the role of cGMP degradation by phosphodiesterase 5 (PDF 5) on this animal model remains unknown. To investigate the participation of the cGMP pathway in the NO bioavailability in this animal model of hypertension using sildenafil citrate as a pharmacological tool. Male Wistar rats (10-12/group) received oral drugs administration: 1-CONTROL (water ad libidum); 2- L-NAME (65 mg/kg/day); 3- L-NAME (65 mg/kg/day) + Sildenafil (45 mg/kg/day); 4– Sildenafil (45 mg/kg/day). After 8 weeks, the animals were sacrificed and the heart was removed. The heart weight index (HWI, mg/g) and the left ventricular weight index (LVWI, mg/g) were calculated. Fibrotic areas was evaluated by optical microscopy. Table below summarizes data at 8th week: The development of the HC-NOI in rats involves the cGMP pathway degradation. Clinical Pharmacology & Therapeutics (2004) 75, P13–P13; doi: 10.1016/j.clpt.2003.11.047 vs. Control Group (P <0,05). vs. L-NAME Group (P <0,05). More... »

PAGES

p13-p13

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URI

http://scigraph.springernature.com/pub.10.1016/j.clpt.2003.11.047

DOI

http://dx.doi.org/10.1016/j.clpt.2003.11.047

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020076954


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