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AIMS: The objective of this study was to evaluate the expression of bladder receptors in patients with defunctionalized bladder (DB) and to assess voiding behavior after refunctionalization. METHODS: A total of 68 pretransplant patients were divided in two groups: DB (diuresis <300 mL/24 h; n = 33) and NDB (non-DB; diuresis ≥300 mL/24 h; n = 35). A sample of mucosa and detrusor at the site of the future ureteral implantation was collected. The following receptors were assessed by real-time polymerase chain reaction (qRT-PCR): M2 , M3 , α1D , ß3 , P2X2 , P2X3 , TRPV1, TRPV4, TRPA1, and TRPM8. At 3, 6, and 12 months after transplant patients answered IPSS and ICIQ-OAB questionnaires and filled a 3-day 24 h frequency/volume chart (FVC) at 6 and 12 months. RESULTS: The expression of all receptors in the mucosa and in the detrusor was similar in both groups, except from α1D , which was overexpressed in the detrusor of DB relatively to NDB group. ICIQ-OAB symptom score was similar between the groups at 3, 6, and 12 months. There was a reduction of this score in both groups with time. The same pattern was found for IPSS score. Bother scores were similar between groups. No difference was observed for all FVC parameters between DB and NDB patients. CONCLUSION: Gene expression of bladder receptors involved in micturition control was similar in patients with or without DB. Bladder behavior had a similar pattern independently of pretransplant residual diuresis. These findings question the relevance of the term DB in pretransplant patients.

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Objective: To evaluate autonomic and cardiovascular function, as well as inflammatory and oxidative stress markers in ob/ob female mice. Methods: Metabolic parameters, cardiac function, arterial pressure (AP), autonomic, hormonal, inflammatory, and oxidative stress markers were evaluated in 12-weeks female wild-type (WT group) and ob/ob mice (OB group). Results: OB animals showed increased body weight, blood glucose, and triglyceride levels, along with glucose intolerance, when compared to WT animals. Ejection fraction (EF) and AP were similar between groups; however, the OB group presented diastolic dysfunction, as well as an impairment on myocardial performance index. Moreover, the OB group exhibited important autonomic dysfunction and baroreflex sensitivity impairment, when compared to WT group. OB group showed increased Angiotensin II levels in heart and renal tissues; decreased adiponectin and increased inflammatory markers in adipose tissue and spleen. Additionally, OB mice presented a higher damage to proteins and lipoperoxidation and lower activity of antioxidant enzymes in kidney and heart. Correlations were found between autonomic dysfunction with angiotensin II and inflammatory mediators, as well as between inflammation and oxidative stress. Conclusions: Our results showed that female adult ob/ob mice presented discrete diastolic dysfunction accompanied by autonomic disorder, which is associated with inflammation and oxidative stress in these animals.

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Chronic spinal cord injury (SCI) is often associated with reductions in left ventricular (LV) diastolic function. Impairments in sympathetic activity and activation of the renin-angiotensin system are reported in SCI individuals and may hypothetically be implicated in this association. Hence, the present study verified the relationship between these two neuro-hormonal and cardiac functional and structural characteristics in SCI individuals. Twenty-two men with SCI (injury level above T6 and no voluntary motion below the injury) and 11 able-bodied men were evaluated by clinical, hemodynamic, laboratory, and echocardiographic analysis and had plasmatic renin, angiotensin I (ANGI), angiotensin II (ANGII), angiotensin 1-7 (ANG1-7), and noradrenaline levels measured. SCI subjects had lower noradrenaline (p = 0.003) and higher ANG1-7 (p = 0.009), but similar renin, ANGI, and ANGII levels when compared with able-bodied individuals. In SCI individuals, results of multi-variable analysis showed that higher Em, a marker of better LV diastolic function, was directly associated with ANG1-7 (p = 0.05) or ANG1-7/ANGII ratio (p = 0.007), whereas lower noradrenaline levels were independently associated with worse LV diastolic function, as assessed by E/Em ratio (p = 0.028). In conclusion, these results suggest that reduced sympathetic activity and expression of ANG1-7 may be involved in SCI-related diastolic dysfunction.

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BACKGROUND: The increased prevalence of asthma and allergic diseases in westernized societies has been associated with increased intake of diets rich in n-6 fatty acids (FAs) and poor in n-3 FAs. This study aimed to analyze the prophylactic effects of treatment with a soybean oil-rich diet (rich in n-6) or fish oil (rich in n-3) in an allergic airway inflammation model on lung inflammation score, leukocyte migration, T-helper cell (Th)-2 (interleukin [IL]-4, IL-5) and Th1 (interferon [IFN]-γ, tumor necrosis factor-α) cytokines, lipoxin A4, nitric oxide, bradykinin, and corticosterone levels in bronchoalveolar lavage (BAL) or lungs. METHODS: Male Wistar rats fed with soybean oil- or fish oil-rich diet or standard rat chow were sensitized twice with ovalbumin-alumen and challenged twice with ovalbumin aerosol. The BAL and lungs were examined 24 hours later. RESULTS: Both diets, rich in n-6 or n-3 FAs, impaired the allergic lung inflammation and reduced leukocyte migration, eosinophil and neutrophil percentages, and IL-4/IL-5/bradykinin levels in BAL and/or lungs, as well as increased the nitric oxide levels in BAL. The soybean oil-rich diet additionally increased the levels of lipoxin A4 and corticosterone in the lungs. CONCLUSION: Data presented demonstrated that the n-6 FA-rich diet had protective effect upon allergic airway inflammation and was as anti-inflammatory as the n-3 FA-rich diet, although through different mechanisms, suggesting that both diets could be considered as complementary therapy or a prophylactic alternative for allergic airway inflammation.

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INTRODUCTION: Tonin is an enzyme that is able to generate angiotensin II (Ang II) from angiotensin I (Ang I) or directly from angiotensinogen. Our goal was to characterize the renal renin-angiotensin system in transgenic mice that express rat tonin (TGM`(rTon)). MATERIALS AND METHODS: Mice were euthanized and the kidneys removed for analysis. Tonin activity was evaluated by radioimmunoassay and angiotensin I-converting enzyme (ACE) activity by HPLC. Tonin, ACE and angiotensin II-converting enzyme (ACE2) expression was analyzed by Western blotting. RESULTS: Tonin activity was significantly increased in TGM`(rTon) compared to their respective wild-type (WT) littermates (1.7 ± 0.21 vs 0.11 ± 0.02 nmol of Ang II/min/mg of protein). Tonin activity had a strong positive correlation with tonin expression in both TGM`(rTon) and their respective wild-type littermates. The ACE activity and expression levels of 65-kDa N-domain angiotensin I-converting enzyme isoform were significantly increased in the TGM`(rTon) when compared with WT. ACE2 expression levels were statistically significantly higher in the TGM`(rTon) when compared with WT. Angiotensin 1-7 (Ang(1-7)) and Ang I levels were significantly lower in the TGM`(rTon). CONCLUSIONS: We suggest that the environment of tonin abundance may increase N-domain ACE activity liberated by a secretase able to cleave somatic ACE.

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UNLABELLED: Recent findings suggest that low-birth-weight children with current obesity are more likely to have higher systolic blood pressure levels and impaired ß-cell function than those who are obese with normal birth weight. It seems possible, however, that concurrent low birth weight with excess weight gain can exacerbate other risk factors for cardiometabolic diseases. The purpose of this study is to investigate the influence of birth weight on the lipid/apolipoprotein profile, visfatin levels, and insulin parameters in overweight/obese children. A cross-sectional study of 68 overweight/obese children was conducted. Among these children, 28 were identified with low birth weight and 40 were of normal birth weight. Blood lipid profile, apolipoproteins, visfatin, glucose, and insulin were measured. Our results show that systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels, triglycerides (TG), very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDLc), apolipoprotein B and E, insulin, apolipoprotein B/A1 ratio, and homeostasis model assessment insulin resistance (HOMA-IR) were significantly elevated in overweight/obese low-birth-weight (LBW) children. There was a significant association of the SBP levels with TG (P=0.027), LDLc (P=0.001), HOMA-IR (P<0.001), apolipoprotein B (P=0.001), and apolipoprotein E (P=0.039). CONCLUSION: Our findings suggest that LBW children with overweight or obesity have an additional risk factor for both atherogenic and insulinogenic profile.

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Several clinical and experimental studies support the hypothesis that foetal programming is an important determinant of nephropathy, hypertension, coronary heart disease, and type 2 diabetes during adulthood. In this paper, the renal repercussions of foetal programming are emphasised, and the physiopathological mechanisms are discussed. The programming of renal diseases is detailed based on the findings of kidney development and functional parameters.

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BACKGROUND: The human angiotensin-converting enzyme (ACE) gene contains a polymorphism consisting of either an insertion (I) or a deletion (D) of a 287 bp Alu repetitive sequence in intron 16. The potential role of ACE polymorphism in the risk of developing hypertension or other cardiovascular disorders has not been determined in relation to birth weight (BW). METHODS: The ACE genotype and plasma ACE activity were determined in 167 children. Among these children, 60 were identified with low BW (LBW), and 107 were of normal BW (NBW). RESULTS: ACE activity levels were significantly elevated in LBW children compared with the NBW group (P < 0.001). There was a significant association of the ACE activity with systolic blood pressure (SBP) levels in our population (P < 0.001). Among the ACE genotypes, no significant differences were found with respect to BW (P = 0.136). However, our results revealed that LBW children had a higher D allele frequency than NBW children (P = 0.036). When analyzed by quartiles of SBP or ACE activity, we found a greater frequency of both the LBW children and those carrying the DD genotype in the highest quartiles of these parameters, whereas the NBW children tended to be in the lowest quartile (P < 0.001). Similar results were observed with the heterozygote ID children after categorization by quartiles of both SBP (P < 0.001) and ACE activity (P = 0.004). CONCLUSIONS: The ACE I/D polymorphism, especially the DD genotype, can be interpreted as a major factor in association between LBW and high BP levels.

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BACKGROUND: G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. In this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensive mice. METHODS: Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 µg/kg/day) or vehicle for 14 days. RESULTS: Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150±5 vs. 129±2 mmHg, p<0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. The clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50±0.02 vs. 0.66±0.01, p<0.05). The infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSF mice. Administration of G-CSF protected the clipped kidney from apoptosis. CONCLUSION: Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia.

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