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Research paper thumbnail of Resurgence of carbon monoxide: an endogenous gaseous vasorelaxing factor

Canadian Journal of Physiology and Pharmacology, 1998

Carbon monoxide (CO) is an endogenously generated gas that may play an important physiological ro... more Carbon monoxide (CO) is an endogenously generated gas that may play an important physiological role in the regulation of vascular tone. The CO-induced vasorelaxation, as a result of a direct action on vascular smooth muscles, has been demonstrated in many cases. Three major cellular mechanisms are proposed to explain the vasorelaxing effect of CO. These include the activation of soluble guanylyl cyclase, stimulation of various types of K channels, and inhibition of the cytochrome P450 dependent monooxygenase system in vascular smooth muscle cells. An interaction between CO and nitric oxide may also significantly contribute to the fine tuning of vascular tone. Furthermore, alterations in either the endogenous production of CO or the vascular responsiveness to CO have been encountered in several pathophysiological situations. A better understanding of the vascular effects of CO and the underlying cellular and molecular mechanisms will pave the way for the establishment of the role played by CO in vascular physiology and pathophysiology.

Research paper thumbnail of Real-time soft shadows in dynamic scenes using spherical harmonic exponentiation

ACM Transactions on Graphics, 2006

Research paper thumbnail of Real-time KD-tree construction on graphics hardware

ACM Transactions on Graphics, 2008

Research paper thumbnail of Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system

Proceedings of The National Academy of Sciences, 2004

Research paper thumbnail of Carbon monoxide-induced vasorelaxation and the underlying mechanisms

British Journal of Pharmacology, 1997

Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tis... more Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tissues which were precontracted with phenylephrine or U-46619. This vasorelaxing effect of CO was independent of the presence of the intact endothelium.The CO-induced vasorelaxation was partially inhibited by the blockade of either the cyclicGMP pathway or big-conductance calcium-activated K (KCa) channels. When both the cyclicGMP pathway and KCa channels were blocked, the CO-induced vasorelaxation was completely abolished.Incubation of vascular tissues with hemin, in order to enhance the endogenous production of CO, suppressed the phenylephrine-induced vasocontraction in a time- and concentration-dependent manner. The hemin-induced suppression of the vascular contractile response to phenylephrine was abolished after the vascular tissues were co-incubated with either oxyhaemoglobin or zinc protoporphyrin-IX, suggesting an induced endogenous generation of CO from vascular tissues.The effect of hemin incubation on vascular contractility did not involve the endogenous generation of nitric oxide.Our results suggest that CO may activate both a cyclicGMP signalling pathway and KCa channels in the same vascular tissues, and that the endogenously generated CO may significantly affect the vascular contractile responses.Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tissues which were precontracted with phenylephrine or U-46619. This vasorelaxing effect of CO was independent of the presence of the intact endothelium.The CO-induced vasorelaxation was partially inhibited by the blockade of either the cyclicGMP pathway or big-conductance calcium-activated K (KCa) channels. When both the cyclicGMP pathway and KCa channels were blocked, the CO-induced vasorelaxation was completely abolished.Incubation of vascular tissues with hemin, in order to enhance the endogenous production of CO, suppressed the phenylephrine-induced vasocontraction in a time- and concentration-dependent manner. The hemin-induced suppression of the vascular contractile response to phenylephrine was abolished after the vascular tissues were co-incubated with either oxyhaemoglobin or zinc protoporphyrin-IX, suggesting an induced endogenous generation of CO from vascular tissues.The effect of hemin incubation on vascular contractility did not involve the endogenous generation of nitric oxide.Our results suggest that CO may activate both a cyclicGMP signalling pathway and KCa channels in the same vascular tissues, and that the endogenously generated CO may significantly affect the vascular contractile responses.

Research paper thumbnail of Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3

Research paper thumbnail of H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine Lyase

Research paper thumbnail of 2012 Pepsi Co Annual Report

Research paper thumbnail of Resurgence of carbon monoxide: an endogenous gaseous vasorelaxing factor

Canadian Journal of Physiology and Pharmacology, 1998

Carbon monoxide (CO) is an endogenously generated gas that may play an important physiological ro... more Carbon monoxide (CO) is an endogenously generated gas that may play an important physiological role in the regulation of vascular tone. The CO-induced vasorelaxation, as a result of a direct action on vascular smooth muscles, has been demonstrated in many cases. Three major cellular mechanisms are proposed to explain the vasorelaxing effect of CO. These include the activation of soluble guanylyl cyclase, stimulation of various types of K channels, and inhibition of the cytochrome P450 dependent monooxygenase system in vascular smooth muscle cells. An interaction between CO and nitric oxide may also significantly contribute to the fine tuning of vascular tone. Furthermore, alterations in either the endogenous production of CO or the vascular responsiveness to CO have been encountered in several pathophysiological situations. A better understanding of the vascular effects of CO and the underlying cellular and molecular mechanisms will pave the way for the establishment of the role played by CO in vascular physiology and pathophysiology.

Research paper thumbnail of Real-time soft shadows in dynamic scenes using spherical harmonic exponentiation

ACM Transactions on Graphics, 2006

Research paper thumbnail of Real-time KD-tree construction on graphics hardware

ACM Transactions on Graphics, 2008

Research paper thumbnail of Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system

Proceedings of The National Academy of Sciences, 2004

Research paper thumbnail of Carbon monoxide-induced vasorelaxation and the underlying mechanisms

British Journal of Pharmacology, 1997

Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tis... more Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tissues which were precontracted with phenylephrine or U-46619. This vasorelaxing effect of CO was independent of the presence of the intact endothelium.The CO-induced vasorelaxation was partially inhibited by the blockade of either the cyclicGMP pathway or big-conductance calcium-activated K (KCa) channels. When both the cyclicGMP pathway and KCa channels were blocked, the CO-induced vasorelaxation was completely abolished.Incubation of vascular tissues with hemin, in order to enhance the endogenous production of CO, suppressed the phenylephrine-induced vasocontraction in a time- and concentration-dependent manner. The hemin-induced suppression of the vascular contractile response to phenylephrine was abolished after the vascular tissues were co-incubated with either oxyhaemoglobin or zinc protoporphyrin-IX, suggesting an induced endogenous generation of CO from vascular tissues.The effect of hemin incubation on vascular contractility did not involve the endogenous generation of nitric oxide.Our results suggest that CO may activate both a cyclicGMP signalling pathway and KCa channels in the same vascular tissues, and that the endogenously generated CO may significantly affect the vascular contractile responses.Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tissues which were precontracted with phenylephrine or U-46619. This vasorelaxing effect of CO was independent of the presence of the intact endothelium.The CO-induced vasorelaxation was partially inhibited by the blockade of either the cyclicGMP pathway or big-conductance calcium-activated K (KCa) channels. When both the cyclicGMP pathway and KCa channels were blocked, the CO-induced vasorelaxation was completely abolished.Incubation of vascular tissues with hemin, in order to enhance the endogenous production of CO, suppressed the phenylephrine-induced vasocontraction in a time- and concentration-dependent manner. The hemin-induced suppression of the vascular contractile response to phenylephrine was abolished after the vascular tissues were co-incubated with either oxyhaemoglobin or zinc protoporphyrin-IX, suggesting an induced endogenous generation of CO from vascular tissues.The effect of hemin incubation on vascular contractility did not involve the endogenous generation of nitric oxide.Our results suggest that CO may activate both a cyclicGMP signalling pathway and KCa channels in the same vascular tissues, and that the endogenously generated CO may significantly affect the vascular contractile responses.

Research paper thumbnail of Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3

Research paper thumbnail of H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine Lyase

Research paper thumbnail of 2012 Pepsi Co Annual Report

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