Oxygen radical—mediated vascular injury selectively inhibits receptor-dependent release of nitric oxide from canine coronary arteries

Seccombe, John F.; Pearson, Paul J.; Schaff, Hartzell V.

doi:10.1016/s0022-5223(94)70096-6

Cited by 43 publications

(11 citation statements)

References 21 publications

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“…However, our observations that muscarinic agonists are more sensitive to endothelial dysfunction are consistent with the finding that atheroma-like lesions have a greater effect on the relaxant responses to ACh than other endothelium-dependent dilators (Arthur & Dusting, 1992). Furthermore, Seccombe et al (1994) have reported that generation of oxygen radicals in vitro impairs endothelium-dependent relaxation to ACh and adenosine diphosphate but not Methoxamine (nmol) Figure 4 The effect of 30 min low flow-ischaemia and 15 min reperfusion on the responses to endothelium-dependent vasodilators in rat coronary resistance arteries preconstricted with U46619. The vasodilator responses to acetylcholine (a, control n =9, ischaemia n =6) and carbachol (b, control n = 4, ischaemia n = 4) but not to bradykinin (c, control n = 5, ischaemia n = 6) or histamine (d, control n = 5, ischaemia n = 6) were significantly impaired by 30 min low flow ischaemia-reperfusion (0) as compared to responses in control hearts (0).…”

Section: Discussionsupporting

confidence: 89%

The effect of ischaemia on endothelium‐dependent vasodilatation and adrenoceptor‐mediated vasoconstriction in rat isolated hearts

Pannangpetch

Woodman

1996

British J Pharmacology

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1 The aim of this study was to investigate whether global ischaemia and reperfusion in rat isolated hearts affects endothelium-dependent vasodilatation and adrenoceptor-mediated vasoconstriction. In addition, it was first determined whether inhibition of the actions of nitric oxide (NO) influenced the responses to a-adrenoceptor agonists in the rat coronary vasculature.2 In rat isolated, Langendorff perfused hearts, inhibition of NO with haemoglobin (Hb, 6 gM) significantly inhibited the vasodilator responses to the endothelium-dependent vasodilators, acetylcholine (ACh, 3-100 pmol), carbachol (CCh, 10-300 pmol), bradykinin (Bk, 1-30 pmol) and histamine (0.3-10 nmol) but did not affect responses to the endothelium-independent vasodilator, sodium nitroprusside (SNP, 0.01-1 nmol). 3 Inhibition of the action of NO by Hb significantly enhanced the vasoconstrictor response to the nonselective a-adrenoceptor agonist, noradrenaline (NA, 0.1-1O nmol) and the a2-adrenoceptor agonist, B-HT 920 (0.001 -1 imol) but had no effect on the vascular response to the ac-adrenoceptor agonist, methoxamine (MTX, 10-300 nmol). 4 In the perfused hearts ischaemia, induced by 30 min perfusion at 5% of the normal rate of flow, followed by 15 min of reperfusion (ischaemia/reperfusion) selectively impaired the vasodilator responses to ACh and CCh which act by muscarinic receptor stimulation but did not affect responses to the other endothelium-dependent vasodilators Bk and histamine or to the endothelium-independent dilator SNP. 5 After ischaemia/reperfusion the coronary vasoconstrictor responses to B-HT 920 were slightly but significantly enhanced whereas the responses to NA and MTX were unaffected. 6 Thus, in the rat isolated heart, low flow induced-ischaemia and reperfusion causes a selective impairment of muscarinic receptor-mediated vasodilatation but does not impair responses to all endothelium-dependent vasodilators. Enhanced constrictor responses to noradrenaline and B-HT 920 in the presence of Hb indicates that endogenous NO modulates the constriction of coronary resistance vessels in response to stimulation of a2-adrenoceptors. Ischaemia and reperfusion in this isolated vascular bed caused only a small increase in the coronary vasoconstrictor response to cx2-adrenoceptor stimulation. It appears that in the rat isolated heart the degree of endothelial dysfunction caused by ischaemia/reperfusion is insufficient to cause a functionally significant change in a-adrenoceptormediated constriction.

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Section: Discussionsupporting

confidence: 89%

The effect of ischaemia on endothelium‐dependent vasodilatation and adrenoceptor‐mediated vasoconstriction in rat isolated hearts

Pannangpetch

Woodman

1996

British J Pharmacology

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“…In accordance with these observations, the findings of the present study also demonstrated that 60 min of ischaemia followed by 60 min of reperfusion caused a marked decrease in bladder contractility upon stimulation with carbachol. Seccombe et al (1994) reported the possibility that oxygen-derived radicals during ischaemia impair the signal transduction system in Contraction (%) Figure 1 Concentration-response curves obtained by cumulative addition of carbachol (10 −8 -10 −4 M) to rat bladder strips obtained from experimental groups. Ischaemia/reperfusion (I/R) was performed by ischaemia of the abdominal aorta for 60 min followed by reperfusion for 60 min.…”

Section: Myeloperoxidase Activitymentioning

confidence: 99%

Montelukast reduces ischaemia/reperfusion-induced bladder dysfunction and oxidant damage in the rat

Şener

Şehirli

Toklu

et al. 2007

Journal of Pharmacy and Pharmacology

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The present study aimed to investigate the possible beneficial effects of the cysteinyl leukotriene-1 receptor antagonist montelukast on contractility and oxidant damage after ischaemia/reperfusion (I/R) of rat urinary bladder. The abdominal aorta of Sprague-Dawley rats was occluded to induce I/R. Montelukast (10 mg kg(-1)) or saline was administered intraperitoneally before I/R. In the sham-operated group, the abdominal aorta was left intact and the animals were treated with montelukast or saline. After decapitation, the bladder was removed and the tissue was either used for functional studies or stored for biochemical assays. In the I/R group, the isometric contractile responses of the bladder strips to carbachol (10(-8)-10(-4) M) were lower than those of the control group and were reversed by treatment with montelukast. Lipid peroxidation and myeloperoxidase activity of the bladder tissues in the I/R group were greater than in the sham-operated group. Montelukast treatment in the I/R group decreased these parameters compared with I/R alone. Similarly, the significant decrease in tissue glutathione level in the I/R group compared with controls was also prevented by montelukast. Treatment with montelukast almost completely reversed the low contractile responses of rat urinary bladder to carbachol and prevented oxidative tissue damage following I/R.

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“…Several correlations have been drawn so far to connect the possible mechanism for hypertension in response to iNOS. In recent literature, two major possibilities have been tied to increased vasoreactivity and thrombogenesis i) faulty action of peroxynitrite-mediated endothelial NO release, thereby impairing normal vasoreactivity (Seccombe, Pearson, & Scha , 1994) and ii) superoxide stimulate platelet adhesion and aggregation binding with peroxynitrite interactions (Salvemini, Nucci, Sneddon, & Vane, 1989;Seccombe et al, 1994). ese two possible theories make change in thrombogenesis and vasoreactivity thus progressing the aggregation of unstable plaque.…”

Section: Hypertension Biologymentioning

confidence: 99%

Targeting inducible Nitric Oxide Synthase (iNOS) in the prevention of vascular damage and cardiac inflammation in CVD

Chowdhury¹,

Tisha²,

Sarker³

et al. 2018

J. Angiother.

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Vascular damage and subsequent cardiac failure due to immune cytokines is steadily increasing the morbidity of cardiovascular diseases (CVD), making them the leading cause of death globally. Nevertheless, improper diagnosis is an important hurdle in case management. Free radicals are one of major factors in producing vascular abnormalities in CVD. Additionally, some other factors such as high blood pressure, myocardial injuries, vascular damage, ventricular hypertrophy, cardiac fibrosis and myocardial necrosis are also the results of free radical-mediated abnormal cardiac activity/function. Of note, Nitric Oxide Synthase (iNOS) is produced in the body at an elevated rate in the presence of free radicals which has been shown to lead to cardiac issues. Furthermore, iNOS is also increased due to cytoplasmic stress, faulty DNA replication and membrane potential impairment. Moreover, abnormal cardiac rhythm has also been reported to be linked to the presence of iNOS. iNOS can also lead to abnormal cardiac function through inhibition of mitochondrial activity and production of pro-inflammatory cytokines. The molecular mechanism of iNOS that leads to CVD is comprehensively summarized in this review so as to aid in drug discovery strategies for the treatment of CVD.

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Oxygen radical—mediated vascular injury selectively inhibits receptor-dependent release of nitric oxide from canine coronary arteries

Cited by 43 publications

References 21 publications

The effect of ischaemia on endothelium‐dependent vasodilatation and adrenoceptor‐mediated vasoconstriction in rat isolated hearts

The effect of ischaemia on endothelium‐dependent vasodilatation and adrenoceptor‐mediated vasoconstriction in rat isolated hearts

Montelukast reduces ischaemia/reperfusion-induced bladder dysfunction and oxidant damage in the rat

Targeting inducible Nitric Oxide Synthase (iNOS) in the prevention of vascular damage and cardiac inflammation in CVD

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