Endothelium-Derived Contracting Factor in Carotid Artery of Hypertensive Dahl Rats

Zhou, Ming-Sheng; Nishida, Yasuhiro; Chen, Qing‐Hui; Kosaka, Hiroaki

doi:10.1161/01.hyp.34.1.39

Cited by 33 publications

(21 citation statements)

References 33 publications

(30 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…49 Enhanced formation of 8-isoprostane has been associated with several cardiovascular risk factors 50 and has been found to correlate with in vivo thromboxane A 2 biosynthesis. 39,45 In line with these reports, we previously reported that high salt induces acetylcholine-induced contraction caused by endotheliumderived contraction factor, which may be thromboxane A 2 and/or prostaglandin H 2 , in carotid and renal arterial rings but not aorta of hypertensive DS rats, 19 and L-arginine supplementation diminished the contraction. 20 Actually, we showed in this study that high salt loading increases urinary thromboxane B 2 (a stable metabolite of thromboxane A 2 ) excretion ( Figure 7B), which was reduced by L-arginine supplementation.…”

Section: Discussionsupporting

confidence: 71%

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

et al. 2003

Self Cite

View full text Add to dashboard Cite

Abstract-Derangements in the production and degradation of reactive oxygen species (ROS) as well as nitric oxide (NO) have been implicated in cardiovascular diseases. We explored how supplementation with L-arginine, an NO synthase substrate, restores such derangements of ROS/NO systems in Dahl salt-sensitive, hypertensive (DS) rats. We detected an increase of NADPH oxidase activity, a key enzyme that produces superoxide, in the membrane fraction of the renal cortex derived from DS rats loaded with high salt for 4 weeks; high salt loading also remarkably increased urinary H 2 O 2 , 8-isoprostane, and thromboxane B 2 excretion and decreased plasma NO end products. These changes from high salt loading were counteracted by oral L-arginine supplementation. We further examined expression patterns of NADPH oxidase subunits in renal cortex derived from these animals. High salt loading increased gp91phox and p47phox but not p22phox or Rac1 or mRNA abundance, which were counteracted with L-arginine supplementation. Western blot analyses after subcellular fractionation revealed that L-arginine supplementation distinctly decreases membrane localization of p47phox protein, as it decreases total expression of Rac1 protein in DS rats with high salt loading. These results disclose that high salt loading causes a deficiency in available L-arginine amounts for NO synthases and induces NADPH oxidase activation in the renal cortex of DS rats, which L-arginine supplementation markedly restores. Since superoxide rapidly eliminates NO, which inhibits sodium reabsorption in the cortical collecting duct, superoxide production caused by upregulated NADPH oxidase activity in the renal cortex of high salt-loaded DS rats may accelerate sodium reabsorption and hypertension. Key Words: rats, Dahl Ⅲ arginine Ⅲ hypertension, sodium-dependent Ⅲ nitric oxide Ⅲ cardiovascular diseases R ecent studies have revealed significant associations between the pathogenesis of numerous cardiovascular diseases, including hypertensive states, and the increase in reactive oxygen species (ROS) and/or the decrease in nitric oxide (NO). [1][2][3] Complete understanding of such derangements in ROS/NO systems has been prevented by the fact that mammalian organs are provided with multiple layers of complicated enzymatic as well as nonenzymatic machineries that deal with ROS/NO. 4,5 Among such machineries, NADPH oxidase, which was originally known to produce a large amount of superoxide anion to kill bacteria in neutrophils, 6 has attracted much attention as a potentially important player in a wide array of cardiovascular disorders. Although NADPH oxidase in the nonphagocytic cells has been less well characterized, physiologically relevant low generation of ROS and neutrophillike expression of NADPH oxidase subunits is present in vascular tissues, 7,8 which is activated by pulsatile stretch, 9 platelet-derived growth factor, 10 and angiotensin II. 1,[11][12][13][14][15] These studies, when taken together, suggest that NADPH oxidase may exert broader actions in cardi...

show abstract

Section: Discussionsupporting

confidence: 71%

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

et al. 2003

Self Cite

View full text Add to dashboard Cite

show abstract

“…Increased COX-2 prostanoids in hypertension Alvarez et al 775 Prostanoids acting on TP receptors have been described as implicated in the altered response to several vasoconstrictors in aorta from different animal models of hypertension [2,3,21,34,35]. In agreement, the TP receptor blocker SQ 29,548 reduced the phenylephrine-induced contraction in segments from both strains, and this reduction was markedly greater in aorta from SHR, as also occurred with indomethacin, NS 398 and dexamethasone.…”

Section: Discussionmentioning

confidence: 89%

“…However, neither furegrelate nor OKY 046, both TxA 2 synthase inhibitors, modified the response to phenylephrine, suggesting that prostanoids other than TxA 2 , by acting on the TP receptor, contribute to the constrictor effect of phenylephrine on aortic segments. Contractile prostanoids other than TxA 2 have also been involved in the vasoconstrictor responses induced by angiotensin II in aorta from rats with aortic-coarctation-induced hypertension [34], while TxA 2 has been implicated in the contraction induced by endothelin [2], A23187 [2] and acetylcholine [35].…”

Section: Discussionmentioning

confidence: 99%

Hypertension increases the participation of vasoconstrictor prostanoids from cyclooxygenase-2 in phenylephrine responses

Álvarez¹,

Briones²,

Balfagón

et al. 2005

Journal of Hypertension

View full text Add to dashboard Cite

show abstract

“…As observed in Figure 2, the percentage of the area under the curve was greater after the exercise, suggesting that acute resistance exercise decreased the vasoconstrictor prostanoid release in conductance vessels. The endothelial dysfunction present in arterial hypertension evokes an increase in vasoconstrictor prostanoid production, 35-38 and a single resistance exercise session has an important impact on vascular function improvement, because it decreases the vasoconstrictor prostanoid release. Moreover, it is well established that NO can regulate the activity of COX enzymes 39 and the activity of NOS is increased when the COX pathway is inhibited by indomethacin.…”

Section: Discussionmentioning

confidence: 99%

A Single Resistance Exercise Session Improves Aortic Endothelial Function in Hypertensive Rats

Faria¹,

Angeli²,

Mello³

et al. 2017

Arquivos Brasileiros De Cardiologia

View full text Add to dashboard Cite

BackgroundPhysical exercise is an important tool for the improvement of endothelial function.ObjectiveTo assess the effects of acute dynamic resistance exercise on the endothelial function of spontaneously hypertensive rats (SHR).MethodsTen minutes after exercise, the aorta was removed to evaluate the expression of endothelial nitric oxide synthase (eNOS), phosphorylated endothelial nitric oxide synthase (p-eNOS1177) and inducible nitric oxide synthase (iNOS) and to generate concentration-response curves to acetylcholine (ACh) and to phenylephrine (PHE). The PHE protocol was also performed with damaged endothelium and before and after NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin administration. The maximal response (Emax) and the sensitivity (EC50) to these drugs were evaluated.Results ACh-induced relaxation increased in the aortic rings of exercised (Ex) rats (Emax= -80 ± 4.6%, p < 0.05) when compared to those of controls (Ct) (Emax = -50 ± 6.8%). The Emax to PHE was decreased following exercise conditions (95 ± 7.9%, p < 0.05) when compared to control conditions (120 ± 4.2%). This response was abolished after L-NAME administration or endothelial damage. In the presence of indomethacin, the aortic rings' reactivity to PHE was decreased in both groups (EC50= Ex -5.9 ± 0.14 vs. Ct -6.6 ± 0.33 log µM, p < 0.05 / Emax = Ex 9.5 ± 2.9 vs. Ct 17 ± 6.2%, p < 0.05). Exercise did not alter the expression of eNOS and iNOS, but increased the level of p-eNOS.ConclusionA single resistance exercise session improves endothelial function in hypertensive rats. This response seems to be mediated by increased NO production through eNOS activation.

show abstract

Endothelium-Derived Contracting Factor in Carotid Artery of Hypertensive Dahl Rats

Cited by 33 publications

References 33 publications

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

Hypertension increases the participation of vasoconstrictor prostanoids from cyclooxygenase-2 in phenylephrine responses

A Single Resistance Exercise Session Improves Aortic Endothelial Function in Hypertensive Rats

Contact Info

Product

Resources

About