Biochemical and Biophysical Research Communications
Hydrogen peroxide: An endogenous smooth muscle cell hyperpolarizing factor☆
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Cited by (95)
Catalase blockade reduces the pressor response to central cholinergic activation
2019, Brain Research BulletinCitation Excerpt :Although ROS may modulate the vascular tone in hypertension (Capettini et al., 2011, 2008; Silva et al., 2012), differently from the effects of icv or iv injection of ATZ on central carbachol-induced pressor response, iv ATZ did not change the hypotensive response to iv carbachol, suggesting that ATZ causes no change in the depressor mechanism activated by carbachol in the endothelial tissue, a mechanism that depends on nitric oxide (NO) (Ignarro et al., 1987; Palmer et al., 1988, 1987; Zhao et al., 2015). In addition to NO, another important endothelium-dependent relaxing factor is H2O2 (Capettini et al., 2011, 2008) that causes both hyperpolarization and vasodilatation in the peripheral and cerebral arteries (Bény and von der Weid, 1991; Iida and Katusic, 2000; Matoba et al., 2002) activating calcium (Ca2+) or K+ channels in the vascular muscle (Barlow et al., 2000; Barlow and White, 1998; Bychkov et al., 1999) and a nonselective cation channel in endothelial cells (Ji et al., 2002). However, the vasodilation produced by iv injection of carbachol was not modified by the injection of ATZ iv, suggesting that the response to carbachol acting in the blood vessels is not modulated by H2O2.
The paracrine control of vascular motion. A historical perspective
2016, Pharmacological ResearchCitation Excerpt :Other candidates on the line were hydrogen peroxide and epoxyeicosatrienoic acids (EETs). Initial evidence showed that the oxygen-derived species, hydrogen peroxide, exhibits hyperpolarizing properties on myocytes but failed to pass the catalase test (forced conversion of hydrogen peroxide into water by this enzyme should inhibit endothelium-dependent hyperpolarization) [76]. However, Matoba and colleagues, nearly a decade later, succeeded in this aspect and presented hydrogen peroxide as a firm candidate for EDHF in a sequence of papers, the first of which was published in 2000 [77] (Fig. 3).
Reactive oxygen species facilitate the EDH response in arterioles by potentiating intracellular endothelial Ca<sup>2+</sup> release
2016, Free Radical Biology and MedicineCitation Excerpt :Liu et al. [11] showed that an endothelium-denuded segment of human coronary artery dilated when it was perfused by the effluent from an upstream endothelium-intact artery subjected to increased shear stress, and that this dilatation was attenuated if an H2O2-scavenging column was interposed between the donor and recipient arteries. The possibility that H2O2 acts as an EDHF is also consistent with observations by other groups that application of exogenous H2O2 opens VSMC BKCa channels [12], hyperpolarizes VSMCs [13] and relaxes a variety of vascular preparations [10,14–16]. The evidence for H2O2 as the primary contributor to the EDHR evoked by bradykinin is also compelling for cerebral arterioles, in which it appears that cyclooxygenase-dependent production of H2O2 causes vasodilation by acting on BKCa channels [16,17].
A role for the sodium pump in H<inf>2</inf>O<inf>2</inf>-induced vasorelaxation in porcine isolated coronary arteries
2014, Pharmacological ResearchCitation Excerpt :However, at higher concentration of H2O2 (1 mM) the pump activity was significantly inhibited. This inhibition could be a possible explanation for the biphasic effects observed in some vessels [49,54] where exogenously applied H2O2 causes initial contraction (Fig. 5C and D) possibly through inhibition of the pump followed by relaxation through hyperpolarization of the vascular smooth muscle cells [14,18,32]. Alternatively, it could also be possible that exposure to high oxidant stress (1 mM) damages the pump [23,55,56].
Oxidant stress and skeletal muscle microvasculopathy in the metabolic syndrome
2012, Vascular PharmacologyEndothelium-derived vasoactive agents, AT1 receptors and inflammation
2011, Pharmacology and TherapeuticsCitation Excerpt :Hydrogen peroxide, a reduction product of superoxide anion dismutation, is either generated spontaneously or catalyzed by the enzyme SOD. It has been shown to induce relaxation and hyperpolarization of VSMC in several vascular beds and as such has properties consistent with EDHF (Beny & von der Weid, 1991; Matoba et al., 2000; Thengchaisri & Kuo, 2003). Its mechanisms of action are still under debate but are likely to involve modulation of Ca2+-activated K+ channels (KCa) (Thengchaisri & Kuo, 2003).
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This work was supported by the Swiss National Foundation, Grant 3,053-0,87.