1. Herein, we report the effects of acute or chronic forced swimming on vascular responsiveness to angiotensin (Ang) II. 2. The possible involvement of locally produced substances, such as nitric oxide (NO) and prostanoids, in these effects were studied in rat thoracic aorta and superior mesenteric arteries. 3. Chronic, but not acute, swimming reduced the efficacy (maximal effect; Emax) of AngII in thoracic aorta and mesenteric arteries, either with intact or denuded endothelium. 4. The efficacy of AngII was reduced in the presence of indomethacin in mesenteric arteries, but not in the aorta, from either control or chronically stressed rats. 5. Treatment with NG-monomethyl-l-arginine reversed the effect of chronic stress on the response to AngII, suggesting that chronic stress may increase non-endothelial NO activity in both the aorta and mesenteric arteries. 6. The effects of acute and chronic stress on vascular reactivity were selective for AngII because no changes were observed on the effects of phenylephrine.

Low intake of BN prior to IR-induced kidney injury improves renal function by inhibition of macrophage infiltration and oxidative stress.

This study was performed to determine the effect of forced swimming on the vascular responsiveness of the rat superior mesenteric artery to phenylephrine, focusing on the involvement of locally produced substances. Repeated but not single sessions of forced swimming exercise reduced the vasoconstrictor potency of phenylephrine in the studied arteries, regardless of the presence of intact endothelium. No significant changes were observed in the maximal response to phenylephrine. Treatment with indomethacin (1 µM) did not affect the exercise-induced reduction in vascular responsiveness to phenylephrine. However, the reduction of vascular reactivity to phenylephrine due to repeated exercise was no longer observed after treatment with N G -monomethyl-Larginine (L-NMMA, 100 µM). The results suggest that repeated exercise reduces vasomotor responses to phenylephrine in rat superior mesenteric arteries through a nonendothelial nitric oxide (NO)-related mechanism.

No abstract

Under these experimental conditions, the testicular function parameters showed that radiation produced marked damage that was not reversed by treatments. However, gonadal restructuring and recovery of spermatogenesis in treated animals may to reflect attenuation of radiation-induced damages and potential start of recovery.

SummaryRheumatoid arthritis (RA) may promote endothelial dysfunction. This phenomenon requires further investigation, especially in collagen-induced arthritis (CIA), as it is considered the experimental model most similar to RA. The objectives of this study were to identify CIA-induced changes in noradrenaline (NE) and acetylcholine (ACh) responses in mice aortas that may suggest endothelial dysfunction in these animals. Moreover, we characterize CIA-induced modifications in inducible nitric oxide synthase (iNOS) expression in the aortas and cardiac and renal tissues taken from these mice that may be related to possible endothelial dysfunction. Male DBA/1J mice were immunized with 100 lg of emulsified bovine collagen type II (CII) plus complete Freund's adjuvant. Twenty-one days later, these animals received a boost of an additional 100 lg plus incomplete Freund's adjuvant. Fifteen days after the onset of the disease, aortic rings from CIA and control mice were challenged with NE and ACh in an organ bath. In these animals, iNOS was detected through immunohistochemical analysis of aorta, heart and kidneys. Plasma nitrite concentration was determined using the Griess reaction. CIA did not change NE or ACh responses in mice aorta but apparently increased the iNOS expression not only in aorta, but also in cardiac and renal microcirculation. In parallel, CIA reduced nitrite plasma concentration. In mice, CIA appears to increase the presence of iNOS in aorta, as well as in heart and in kidney microcirculation. This iNOS increase occurs apparently in parallel to a reduction of the bioavailability of NO. This phenomenon does not appear to change NE or ACh responses in aorta.

PURPOSE:To analyze the role of hyperbaric oxygen therapy as hepatic preconditioning in rats submitted to hepatic ischemia and reperfusion. METHODS:Wistar rats were randomly divided into three groups: SHAM, rats submitted to surgical stress without hepatic ischemia and reperfusion, I/R, rats submitted to total hepatic pedicle ischemia for 30 min, followed by 5 min of reperfusion; HBOI/R, rats submitted to 60 minutes of hyperbaric oxygen therapy at 2 atm and immediately submitted to the experimental protocol of ischemia and reperfusion.Liver function was assessed by measuring serum alanine aminotransferase and aspartate aminotransferase, as well as mitochondrial function by determining states 3 and 4 of mitochondrial respiration, respiratory control rate and mitochondrial permeability transition (mitochondrial swelling). The results were analyzed by the Mann-Whitney test and all P-values <0.05 were considered significant. RESULTS:There were significant differences in serum aspartate aminotransferase values in groups SHAM vs. HBOI/R, I/R vs HBOI/R, alanine aminotranferase in groups SHAM and I/R; State 3 in SHAM groups vs. I/R, SHAM vs. HBOI/R, State 4 in I/R vs HBOI/R groups, respiratory control rate in SHAM vs I/R groups; mitochondrial swelling in SHAM vs. I/R groups, and SHAM vs HBOI/R. CONCLUSION:Hyperbaric preconditioning improved hepatic mitochondrial function and decreased serum markers of liver injury in the ischemia and reperfusion process.

1. Orchidectomy results in long-term testosterone deprivation similar to that observed in male clinical pathologies, such as hypogonadism and age-related reductions in plasma testosterone concentrations. Although the vascular effects of these sorts of hormone deprivations are known in arteries, they have not been studied to the same extent in veins. 2. The aim of the present study was to determine the effect of orchidectomy, with or without subsequent testosterone replacement (started 23 days after orchidectomy; 10 mg/kg, i.m., testosterone propionate once every 5 days for 3 weeks), on responses of rat isolated portal veins and vena cavae to exogenous phenylephrine (PE). Isolated vessels were mounted in an organ bath and concentration-response curves constructed to PE (10(-10)-10(-4) mol/L), endothelin (ET; 10(-10)-10(-5) mol/L) and KCl (10(-2)-1.2 x 10(-1) mol/L; as a control). 3. Orchidectomy had no effect on contractile responses of either the portal vein or vena cava to KCl. However, orchidectomy enhanced the maximum response (R(max)) of the portal vein, but not the vena cava, to PE. Testosterone replacement had no effect on these responses. The effects of orchidectomy on the R(max) to PE in portal veins were not altered by the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (10(-4) mol/L) alone or combined with 10(-5) mol/L indomethacin (a non-selective cyclo-oxygenase inhibitor), but they were abolished following treatment of isolated vessels with the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 (both at 10(-6) mol/L). Orchidectomy did not alter portal vein responses to the application of exogenous ET. 4. The results of the present study indicate that orchidectomy-induced decreases in plasma testosterone can increase the venoconstrictor effects of PE on the portal vein and that this effect involves activation of both ET(A) and ET(B) receptors by locally produced ET.