L-nitroarginine Methyl Research Articles

Effect of Treadmill Exercise and Ferula gummosa on Myocardial HSP72, Vascular Function, and Antioxidant Defenses in Spontaneously Hypertensive Rats

This study evaluates the effect of treadmill exercise and Ferula gummosa (FG) on heat shock protein (HSP72), biomarkers related to vascular function, and oxidant/antioxidant system in the heart tissue of spontaneously hypertensive rats treated with N(ω)-nitro-l–arginine-methyl ester (l–NAME). Fifty adult male Wistar rats are randomly classified into five groups: treadmill exercise, FG, combination of treadmill exercise + FG, l–NAME, and saline. Treadmill exercise was performed between 25 and 64 minutes at the speed of 15–22 m per minute for 8 weeks and five sessions a week. The FG will be fed through gavage with 90 mg/kg dosage. Hypertension was induced by l–NAME (10 mg/kg) for 8 weeks and six sessions a week. Administration of l–NAME for 8 weeks caused significant increase in HSP72, angiotensin-converting enzyme (ACE), and protein carbonyl (PC), and significant decrease in glutathione peroxidase (GPx) and nitric oxide (NO) level, when compared with the saline group. In contrast, both treadmill exercise and/or FG protocols, in particular, the combined protocol, led to the improvement in HSP72 and balance in oxidant/antioxidant process and inhibited vascular dysfunction, when compared with the l–NAME group. Moreover, no significant differences were detected in the HSP72 level between rats in the treadmill exercise and FG groups. These results provide a rationale for an inhibitory role and a cardioprotective effect of lifestyle related to the health in the attenuation of hypertension-induced cardiotoxicity.

Intestinal Motility in an In Vivo Rat Model of Intestinal Ischemia–Reperfusion With Special Reference to the Effects of Nitric Oxide on the Motility Changes

ABSTRACTBackgroundTo clarify the relation between intestinal ischemia–reperfusion (IR) and dysmotility, the authors investigated changes in the motility pattern in the duodenum and jejunum in an in vivo rat model of IR when artery‐ (and vein‐) fed jejunum was clamped transiently. The authors also studied the effect of nitric oxide on the motility changes in this model by means of the administration of l ‐NAME (NG ‐nitro‐ l ‐arginine methyl ester) or S‐methylisothiourea sulfate (SMT).Materials and MethodsA force transducer was sutured onto the serosal side of the duodenum or jejunum. After a 3‐to 4‐day recovery period, contractions were recorded during periods of preischemia, ischemia (60 minutes), and reperfusion (90 minutes). An intestinal IR was produced by clamping and releasing the mesenteric artery and vein with artery forceps.ResultsIn the jejunum, there was a prolongation in the duration of contraction and there were decreases in the number of contractions (NC) during the IR. When treated with L‐NAME, no decrease in the NC was observed during the 45 to 90 minutes after reperfusion. S‐methylisothiourea sulfate did not affect the IR‐induced motility changes significantly. In the duodenum, there was a prolongation in the duration of contraction and a decrease in the NC and AC only during the reperfusion. l ‐NAME or S‐methylisothiourea sulfate inhibited the decreases in the NC during the reperfusion.ConclusionsIntestinal IR causes motility changes in the ischemic site during the IR and in the nonischemic site during the reperfusion. The IR‐induced motility changes partly depend on nitric oxide production.

Role of the endothelium on the response to adrenoceptor agonists of rabbit aorta during cooling

The role of the endothelium in the effects of cooling on the response to alpha1- and alpha2-adrenoceptor agonists of rabbit aorta was studied. The contractions induced by clonidine (10(-9)-3 x 10(-4) M) and xylazine (10(-7)-10(-3) M) but not phenylephrine (10(-9)-3 x 10(-4) M) and methoxamine (10(-9)-3 x 10(-4) M) were enhanced in endothelium-denuded or N(G)-nitro-L arginine methyl- ester (L-NAME) (10(-5) M) pretreated rabbit aorta. The sensitivity, but not the maximal response, of both alpha1- and alpha2-adrenoceptor agonists was significantly lower at 28 degrees C (cooling) than at 37 degrees C. Endothelium removal did not affect the action of cooling. These results were taken as evidence for the specificity of alpha2-adrenoceptor agonists on the production and release of nitric oxide from vascular endothelium. The results suggest that the endothelium seems to have no role in the cooling-induced responses of both alpha1- and alpha2-adrenoceptors.