Oxytocin Reduces Intravesical Pressure in Anesthetized Female Rats: Action on Oxytocin Receptors of the Urinary Bladder.

Urinary bladder dysfunction affects several people worldwide and shows higher prevalence in women. Micturition is dependent on the Barrington's nucleus, pontine urine storage center and periaqueductal gray matter, but other brain stem areas are involved in the bladder regulation. Neurons in the medulla oblongata send projections to hypothalamic nuclei as the supraoptic nucleus, which synthetizes oxytocin and in its turn, this peptide is released in the circulation. We investigated the effects of intravenous injection of oxytocin (OT) on the urinary bladder in sham and ovariectomized rats. We also evaluated the topical (in situ) action of OT on intravesical pressure (IP) as well as the existence of oxytocin receptors in the urinary bladder. In sham female Wistar rats, anesthetized with isoflurane, intravenous infusion of OT (10 ng/kg) significantly decreased the IP (-47.5 ± 1.2%) compared to saline (3.4 ± 0.7%). Similar effect in IP was observed in ovariectomized rats after i.v. OT (-41.9 ± 2.9%) compared to saline (0.5 ± 0.6%). Topical administration (in situ) of 0.1 mL of OT (1.0 ng/mL) significantly reduced the IP (22.3.0 ± 0.6%) compared to saline (0.9 ± 0.7%). We also found by qPCR that the gene expression of oxytocin receptor is present in this tissue. Blockade of oxytocin receptors significantly attenuated the reduction in IP evoked by oxytocin i.v. or in situ. Therefore, the findings suggest that (1) intravenous oxytocin decreases IP due to bladder relaxation and (2) OT has local bladder effect, binding directly in receptors located in the bladder.

Glutamine supplementation influences the secretory apparatus in the right atrial cardiomyocytes of resistance trained aged rats / A suplementação de glutamina influencia o aparelho secretor dos cardiomiócitos do átrio direito de ratos idosos submetidos a treinamento de resistência / La suplementación de glutamina influye en el aparato secretor de los cardiomiocitos de la aurícula derecha de ratones viejos sometidos a entrenamiento de resistencia

Abstract We investigated the effects of glutamine supplementation on the secretory apparatus of natriuretic peptides in atrial cardiomyocytes of aged rats undergoing resistance training. Two groups of resistance-trained rats were studied: resistance trained, and resistance trained and supplemented with glutamine group. Both groups of rats were trained to climb a 1.1 m vertical ladder with weights tied to their tail. The cardiomyocytes from resistance trained and supplemented rats showed increased density and sectional area of natriuretic peptides granules, higher relative volumes of the mitochondria, endoplasmic reticulum, Golgi complex and nuclear euchromatin, and nuclear pore density compared with resistance trained rats. In conclusion, glutamine supplementation caused hypertrophy of the secretory apparatus in the cardiomyocytes of aged rats undergoing resistance training.

Resumo Foi investigado o efeito da suplementação de glutamina no aparelho secretor de peptídeos natriuréticos dos cardiomiócitos do átrio de ratos idosos submetidos a treinamento de resistencia. Foram estudados dois grupos: grupo de treinamento de resistência e grupo de treinamento de resistência suplementado com glutamina. Os ratos de ambos os grupos escalaram uma escada vertical de 1,1 m com pesos progressivamente maiores atrelados à cauda. Os resultados mostraram que os cardiomiócitos de ratos do grupo treinado e suplementado apresentaram maior densidade e maior área de seção de grânulos de peptideos natriuréticos, maiores volumes relativos de mitocôndrias, retículo endoplasmático, complexo de Golgi e eucromatina nuclear e maior densidade de poros nucleares em comparação com ratos do grupo de treinamento de resistência. Em conclusão, a suplementação com glutamina causou hipertrofia do aparelho secretor dos cardiomiócitos de ratos idosos submetidos ao treinamento de resistência.

Resumen Se investigó la influência de la suplementación de glutamina en el aparato secretor de péptidos natriuréticos de cardiomiocitos auriculares de ratones viejos sometidos a entrenamiento de resistencia. Se formaron dos grupos: grupo de entrenamiento de resistencia y grupo de entrenamiento de resistencia suplementado con glutamina. Los ratones escalaron una escalera vertical de 1,1 m con pesos atados a la cola. Los resultados mostraron que los cardiomiocitos de ratones del grupo de entrenamiento de resistência suplementado presentaron mayor densidad y área de sección de gránulos de péptidos natriuréticos, mayores volúmenes relativos de mitocondrias y de eucromatina nuclear y mayor densidad de poros nucleares en comparación con los ratones del grupo de entrenamiento de resistencia. En conclusión, la suplementación de glutamina causó hipertrofia del aparato secretor en los cardiomiocitos de ratones viejos sometidos al entrenamiento de resistencia.

Resistance Exercise Evokes Changes on Urinary Bladder Function and Morphology in Hypoestrogen Rats.

Serum levels of estrogen decrease at climacterium and directly interfere with the urogenital tract. Urinary bladder (UB) is responsive to hormonal changes, especially estrogen. Resistance exercise elicits benefits on severe chronic diseases. Nevertheless, it is still unclear whether the resistance exercise directly affects the UB in ovariectomized (OVx) rats. This study focused on investigating the effects of resistance exercise on UB function and morphology in OVx and control rats. Adult female Wistar rats (∼250-300 g, 14-16 weeks old) [control (n = 20) and OVx (n = 20)] were divided in the following groups: sedentary (SED), and trained over 1 week (acute), 3 weeks (intermediate), and 10 weeks (chronic). Training was carried out in a ladder, with six bouts in alternate days with 75% of body weight load attached to the tail of the animal. Afterward, the animals were isoflurane anesthetized for evaluation of intravesical pressure (IP) changes upon topical administration of acetylcholine (Ach) and noradrenaline (NE) on the UB. At the end of the experiment, the UB was harvested for histological analysis and stained with hematoxylin-eosin and picrosirius red. Ach increased the IP in both OVx and control rats, whereas NE decreased the IP. However, the acute and intermediate groups showed attenuated responses to Ach and NE, while the chronic groups recovered the responses to Ach and NE close to those observed in SED groups. Acute and intermediate groups also showed decreased thickness of the muscular layer, with a reversal of the process with chronic training. In the OVx groups, the acute training reduced the thickness of the smooth muscle and mucosal layers, whereas chronic training increased it. Urothelium thickness decreased in the OVx SED and acute groups. Collagen type I fibers (CI-F) reduced in OVx SED acute and intermediate groups, while collagen type III fibers (CIII-F) increased in the OVx acute group. In the mucosal layer, the volume density of CFs reduced in OVx rats compared to control groups and chronic training resulted in their recovery. Our data suggest that chronic resistance exercise for 10 weeks reversed the functional and morphological changes caused by hypoestrogenism.

Physical activity on endothelial and erectile dysfunction: a literature review.

Physical inactivity, diabetes, hypertension, dyslipidemia, smoking and obesity were associated with imbalance in oxidative stress, leading to endothelial dysfunction. Such dysfunction is present in both cardiovascular disease (CVD) and erectile dysfunction (ED). ED is the persistent inability to achieve or sustain an erection sufficient for satisfactory sexual performance and is one of the first manifestations of endothelial damage in men with CVD risk factors. The purpose of this article is to review the results of studies involving physical activity, CVD, endothelial dysfunction and ED in order to verify its applicability for improving the health and quality of life of men with such disorders. There is consistent evidence that endothelial damage is intimately linked to ED, and this manifestation seems to be associated with the appearance CVDs. On the other hand, physical activity has been pointed out as an important clinical strategy in the prevention and treatment of CVDs and ED mainly associated with improvement of endothelial function. However, further experimental and clinical prospective investigations are needed to test the role of physical exercises in the modulation of endothelial function and their implications on erectile function and the appearance of CVDs.

The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovariectomized mice.

Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 ( COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice low-density lipoprotein receptor knockout ( LDL-KO) with or without ovariectomy. A total of 15 female C57BL/6 mice and 15 female LDL-KO mice were distributed into 6 groups: sedentary control, sedentary control ovariectomized, trained control ovariectomized, LDL-KO sedentary, LDL-KO sedentary ovariectomized and LDL-KO trained ovariectomized. The ascending part of the aorta was stained with H&E and COX-2 expression was assessed by immunohistochemistry. Results revealed that ovariectomy as well as exercise training were not able to induce histopathological changes in mouse aorta for all groups investigated. LDL-KO mice demonstrated plaque containing cholesterol clefts, foamy histiocytes and mild inflammatory process for all groups indistinctly. Ovariectomy induced a strong immunoexpression in atherosclerosis lesion of LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.

Effects of perinatal protein deprivation and recovery on esophageal myenteric plexus.

AIM: To evaluate effects of pre- and postnatal protein deprivation and postnatal recovery on the myenteric plexus of the rat esophagus. METHODS: Three groups of young Wistar rats (aged 42 d) were studied: normal-fed (N42), protein-deprived (D42), and protein-recovered (R42). The myenteric neurons of their esophagi were evaluated by histochemical reactions for nicotinamide adenine dinucleotide (NADH), nitrergic neurons (NADPH)-diaphorase and acetylcholinesterase (AChE), immunohistochemical reaction for vasoactive intestinal polypeptide (VIP), and ultrastructural analysis by transmission electron microscopy. RESULTS: The cytoplasms of large and medium neurons from the N42 and R42 groups were intensely reactive for NADH. Only a few large neurons from the D42 group exhibited this aspect. NADPH detected in the D42 group exhibited low reactivity. The AChE reactivity was diffuse in neurons from the D42 and R42 groups. The density of large and small varicosities detected by immunohistochemical staining of VIP was low in ganglia from the D42 group. In many neurons from the D42 group, the double membrane of the nuclear envelope and the perinuclear cisterna were not detectable. NADH and NADPH histochemistry revealed no group differences in the profile of nerve cell perikarya (ranging from 200 to 400 microm(2)). CONCLUSION: Protein deprivation causes a delay in neuronal maturation but postnatal recovery can almost completely restore the normal morphology of myenteric neurons.

Effects of combined pre- and post-natal protein deprivation on the myenteric plexus of the esophagus of weanling rats: a histochemical, quantitative and ultrastructural study.

AIM: To evaluate the effects of protein deprivation on the myenteric plexus of the esophagus of weanling rats. METHODS: Pregnant female Wistar rats were divided into 2 groups: nourished (N), receiving normal diet, and undernourished (D), receiving a protein-deprived diet, which continued after birth. At twenty-one days of age, 13 esophagi from each group were submitted to light microscopy and morphometrical analysis employing the NADH diaphorase, NADPH diaphorase and acetylcholinesterase techniques. Three other esophagi from each group were evaluated with transmission electron microscopy (TEM). RESULTS: In both the NADH- and the NADPH-reactive mounts, the neurons of the N mounts were more intensely stained, while in the D esophagi only the larger neurons were reactive. Many myenteric neurons of N were intensely reactive for AChE activity but only a few neurons of D exhibited these aspects. Ultrastructural analysis revealed that the granular reticulum of N showed large numbers of ribosomes aligned on the outer surface of its regularly arranged membrane while the ribosomes of D were disposed in clusters. The chromatin was more homogeneously scattered inside the neuron nucleus of N as well as the granular component of the nucleolus was evidently more developed in this group. Statistically significant differences between N and D groups were detected in the total estimated number of neurons stained by the NADPH technique. CONCLUSION: The morphological and quantitative data shows that feeding with protein-deprived diet in 21-d old rats induces a delay in the development of the myenteric neurons of the esophagus.