Publications by authors named "Mario Angelo Claudino"
Tadalafil, a phosphodiesterase-5 (PDE5) inhibitor, shown to exert a protection to heart failure (HF) associated damage or lower urinary tract symptoms (LUTS). Thus, we investigated the contribution of tadalafil chronic treatment in the alterations of LUTS in HF rats. Male rats were subjected to aortocaval fistula model for HF induction.
View Article and Find Full Text PDFKynurenic acid (KYNA) is derived from tryptophan, formed by the kynurenic pathway. KYNA is being widely studied as a biomarker for neurological and cardiovascular diseases, as it is found in ischemic conditions as a protective agent; however, little is known about its effect after ischemia-reperfusion in the vascular system. We induced ischemia for 30 min followed by 5 min reperfusion (I/R) in the rat aorta for KYNA evaluation using functional assays combined with proteomics.
View Article and Find Full Text PDFArticle Synopsis
- Heart failure (HF) results from various cardiovascular diseases and involves metalloproteinases like MMP9 and TIMP-1, which are crucial for extracellular matrix maintenance and tissue remodeling.
- L-Arginine (LA) treatment shows promising benefits in HF, enhancing vasodilation, restoring endothelial function, and improving muscle contractility.
- In an animal study, LA significantly reduced MMP9 expression after HF, indicating its potential as an adjunct therapy in treating heart failure.
Background: Patients with heart failure (HF) display erectile dysfunction (ED). However, the pathophysiology of ED during HF remains poorly investigated.
Objective: This study aimed to characterize the aortocaval fistula (ACF) rat model associated with HF as a novel experimental model of ED.
Introduction: Hydrochlorothiazide has a negative influence on penile erection but little is known about the mechanism(s) involved.
Aims: To characterize the effects of this diuretic on mouse corpus cavernosum (CC) smooth muscle in vitro and ex vivo.
Methods: CC strips of C57BL/6 mice (12-16 weeks old) were mounted in organ baths containing Krebs-Henseleit solution and tissue reactivity was evaluated.
Article Synopsis
- Urological issues linked to sickle cell disease (SCD) include problems like frequent urination, bedwetting, and urinary infections, but the exact causes for these symptoms are not well understood.
- This study aimed to assess urinary function in a mouse model of SCD, particularly focusing on how their bladders and urinary systems perform.
- Findings revealed that SCD mice showed significantly reduced urine output and bladder contraction capabilities, alongside structural abnormalities in their bladders, indicating dysfunction in the urinary system related to SCD.
Sickle cell anemia is one of the best studied inherited diseases, and despite being caused by a single point mutation in the HBB gene, multiple pleiotropic effects of the abnormal hemoglobin S production range from vaso-occlusive crisis, stroke, and pulmonary hypertension to osteonecrosis and leg ulcers. Urogenital function is not spared, and although priapism is most frequently remembered, other related clinical manifestations have been described, such as nocturia, enuresis, increased frequence of lower urinary tract infections, urinary incontinence, hypogonadism, and testicular infarction. Studies on sickle cell vaso-occlusion and priapism using both in vitro and in vivo models have shed light on the pathogenesis of some of these events.
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- - Priapism is a serious complication of sickle cell disease (SCD) characterized by long-lasting penile erections without sexual desire, and this study explores its underlying mechanisms.
- - The research focused on the role of the NO-cGMP signaling pathway in a mouse model of SCD (SS mice) by analyzing responses of penile tissues to various compounds affecting blood vessel relaxation.
- - Findings indicated that SS mice had significantly enhanced responses to agents like acetylcholine and sodium nitroprusside, suggesting that the signaling pathway related to penile erections is hyperactive in the context of sickle cell disease.