ABSTRACT
Introdução: A hipertensão arterial tem sido um dos maiores problemas de saúde no mundo, com grandes alterações para as doenças cardiovasculares e renais. O tecido ósseo tem função importante no suporte, proteção e locomoção e está sob o controle de fatores sistêmicos como hormônios e fatores locais, entre eles os fatores de crescimento e citocinas. A Fosfatase Ácida Tartarato Resistente (TRAP) é uma enzima que faz parte da família das fosfatases ácidas e apresenta localização intracelular; mais especificamente dentro do compartimento lisossomal de osteoclasto, macrófagos e células dendríticas, tem sido utilizada como um marcador histoquímico da atividade osteoclástica. Objetivos: Avaliar a expressão da proteína TRAP em alvéolos dentários de ratos hipertensos (SHR) e normotensos tratados ou não com atenolol. Métodos: Neste estudo foram utilizados 4 grupos de ratos sendo: 1) W (wistar sem tratamento), 2) WT (wistar tratado com atenolol), 3) S (SHR sem tratamento) e 4) ST (SHR tratado com atenolol), submetidos a exodontia do incisivo superior direito, com eutanásia no 7º, 14º, 21 e 28º dia pós-operatório. A análise dos mecanismos biológicos envolvidos no processo de reparo alveolar foi obtida pela análise da expressão de proteínas TRAP por meio da técnica de imunoistoquímica. Os resultados foram analisados pela média e erro padrão da média e aplicado o teste paramétrico ANOVA, com pos-test de Tukey para avaliar os períodos dentro de cada grupo e entre os grupos, sendo consideradas as diferenças significativas quando p<0,05. Resultados: Os resultados mostraram que a marcação TRAP aumenta em alvéolo dentais de ratos Wistar durante todos os períodos pós operatórios. A marcação TRAP aumenta apenas ao 14o nos dias de reparação alveolar em alvéolo dental de SHR não tratados. O atenolol não altera o processo de reparo alveolar em ratos Wistar, porém o atenolol promoveu a redução da marcação de TRAP em SHR ao 14º dia. Conclusão: A hipertensão aumenta a expressão da proteína TRAP no 14o dia pós-cirúrgico de reparação alveolar e o atenolol promove redução da marcação aumentada de TRAP ao 14º dia pós-cirúrgico em alvéolos de SHR(AU)
Introduction: Arterial hypertension has been one of the world's biggest health problems, with considerable alterations for cardiovascular and renal diseases. The bone tissue has an important role in support, protection and locomotion and is controlled by systemic factors like hormones and local factors, such as growth factors and cytokines. The Tartrate-resistant Acid Phosphatase (TRAP) is an enzyme that belongs to the Acid Phosphatases family and has an intracellular location, more specifically inside the lysosomal compartment of osteoclasts, macrophages and dendritic cells. It has been used as a histochemical marker of the osteoclast activity. Objectives: Evaluate TRAP protein's expression in the dental alveoli of normotensive and hypertensive rats (SHR) treated or not treated with Atenolol. Methods: In this study, four groups of rats were used: 1) W (with no treatment), 2) WT (wistar treated with Atenolol), 3) S (SHR without treatment) and 4) ST (SHR treated with Atenolol), all of which underwent exodontia of the upper right incisor with euthanasia on the 7th, 14th, 21st and 28th day after the operation. The analysis of the biological mechanisms involved in the process of alveolar repair was obtained by the expression of TRAP proteins in the alveolar process through an immunohistochemistry technique. The results were analyzed through the average and its standard error. The parametric test ANOVA was applied with Tukey's posttest were applied to evaluate the periods within each group and between the groups, considering the significant differences when p< 0,05. Results: The results demonstrated that TRAP staining increases in the dental alveoli of Wistar rats during all the post-surgical periods. TRAP staining increases only on the 14th day of alveolar recovery in the dental alveoli of non-treated SHR. Atenolol does not change the process of alveolar repair in Wistar rats, but Atenolol promoted the reduction of TRAP staining among SHR on the 14th day. Conclusion: Hypertension increases the expression of TRAP proteins on the 14th alveolar recovery postsurgical day and Atenolol promotes the reduction of the increased TRAP staining on the 14th postsurgical day in SHR's alveoli(AU)
Subject(s)
Animals , Rats , Atenolol , Hypertension , Surgery, Oral , Tartrate-Resistant Acid Phosphatase , Immunohistochemistry , Rats, Inbred SHR , Tooth SocketABSTRACT
PURPOSE: Overactive bladder is especially common in the elderly, although it is not regarded as a normal part of aging. Thus, we investigated how aging alters the cystometric and detrusor overactivity (DO) parameters and the density of nerve growth factor (NGF) in awake spontaneous hypertensive rats (SHRs) of different ages. METHODS: Three age groups of 12- (n=5), 17- (n=6), and 21- (n=6) week-old SHRs (Oriental Bio Inc.) were used. A catheter was implanted into the bladder to record the intravesical pressure (IVP), and a balloon-fitted catheter was positioned in the abdominal cavity to record the intraabdominal pressure (IAP). Of the IVP elevations above 2 cm H2O, DO was defined as a rise in IVP without a simultaneous change in IAP and was counted during the filling phase. We measured the expression of NGF in the bladders by enzyme-linked immunosorbent assay. RESULTS: Both the body and bladder weights significantly increased with age, but the normalized ratio between those was not changed. As for DO, none of the12-week-old rats showed DO, whereas the other groups did. DO increased significantly with age (P=0.0045 by Mantel-Haenszel trend test), although no significant differences were found in DO frequency or pressure between the 17- and 21-week-old age groups. NGF did not show any significant differences among the three groups. CONCLUSIONS: Our results showed that SHRs begin to shows DO after a certain age, such as 12 weeks of age, and that the occurrence of DO has a close relationship with aging. However, NGF, which is known to be increased in the bladder wall of patients with overactive bladder, did not show any relationship with aging in this study.
Subject(s)
Aged , Animals , Humans , Rats , Abdominal Cavity , Aging , Catheters , Nerve Growth Factor , Rats, Inbred SHR , Urinary Bladder , Urinary Bladder, Overactive , Urodynamics , Weights and MeasuresABSTRACT
Objective: To investigate the arterial baroreflex (ABR)-associated mechanism of losartan in protection of acute cerebral ischemia injury in spontaneously hypertensive rats (SHRs). Methods: Losartan (10 mg·kg -1·d-1) were administered i. g. to SHRs for 2 weeks, and the hemodynamic parameters and the baroreflex sensitivity (BRS) was determined. Then the rats were subjected to middle cerebral arterial (MCA) occlusion to establish acute cerebreal ischemia. The brain samples were obtained, sectioned and stained 24 h later; the infarction area of the brain was measured. Losartan and angiotensin II (Ang II, 100 pmol) were also microinjected into the nucleus of solitary tract (NTS) of rats, and the hemodynamic parameters and BRS were determined 24 h later. Then the rats were subjected to MCA occlusion to establish acute cerebral ischemia injury. The brain infarction area was measured 24 h after operation. Results: Compared to control rats, intragastric administration of losartan improved the ABR function and significantly decreased the infarction area (P<0.05). NTS microinjection of Ang II obviously increased the blood pressure, and decreased BRS value of rats. NTS microinjection of losartan did not change the blood pressure, and significantly improved the ABR function (P<0.05) and alleviated cerebral infarction injury (P<0.05). Conclusion: Losartan can improve the sensitivity of ABR and prevent acute cerebral infarction; NTS might be the target of losartan.