Modulation of cyclic guanosine monophosphate levels in cultured aortic smooth muscle cells by carbon monoxide

Ramos, Kenneth S.; Lin, Hua; McGrath, James J.

doi:10.1016/0006-2952(89)90347-x

Cited by 131 publications

(65 citation statements)

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“…16,18 Furthermore, CO also induces relaxations of vascular tissues 21 and cultured vascular smooth muscle cells. 22 Taken together, it appears that CO and adenosine might have some degree of interaction in the CNS.The purpose of the present study was to provide pharmacological evidence as to whether CO and adenosine are reciprocally released in the NTS. Our results indicate an interaction between CO and adenosine in central cardiovascular regulation.…”

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confidence: 88%

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Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Lin

Hsiao

et al. 2003

Hypertension

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Abstract-Carbon monoxide has been identified as an endogenous biological messenger in the brain. Heme oxygenase catalyzes the metabolism of heme to carbon monoxide and biliverdin. Previously, we have shown the involvement of carbon monoxide in central cardiovascular regulation, baroreflex modulation, and glutamatergic neurotransmission in the nucleus tractus solitarii of rats. We also showed that adenosine increased the release of glutamate in the nucleus tractus solitarii. In this study, we investigated the possible interactions of carbon monoxide and adenosine in the nucleus tractus solitarii. Male Sprague-Dawley rats were anesthetized with urethane, and blood pressure were monitored intra-arterially. Unilateral microinjection of increasing doses of hemin (0.01 to 3.3 nmol), a heme molecule cleaved by heme oxygenase to yield carbon monoxide, produced a significant decrease in blood pressure and heart rate in a dose-dependent manner. In addition, similar cardiovascular effects were observed after injection of adenosine (2.3 nmol). These cardiovascular effects of hemin were attenuated by prior administration of the adenosine receptor antagonist 1,3-dipropyl-8-sulfophenylxanthine. Similarly, pretreatment of the heme oxygenase inhibitor zinc protoporphyrin IX or zinc deuteroporphyrin 2,4-bis glycol also attenuated the depressor and bradycardic effects of adenosine.These results indicate that the interaction between carbon monoxide and adenosine may contribute to the activation of heme oxygenase in central cardiovascular regulation. Key Words: central nervous system Ⅲ blood pressure Ⅲ adenosine Ⅲ heart rate Ⅲ neuroregulators T he gaseous compound carbon monoxide (CO), a new neuromodulator agent, has been shown to play a role as a neurotransmitter. 1 In animals, the predominant source of CO generation is from heme degradation. Heme oxygenase (HO) is the rate-limiting enzyme responsible for the catabolism of heme and subsequent production of CO and biliverdin. Three isoforms of HO have been identified. HO-1, induced by heme and numerous oxidative stressors, is enriched in spleen and liver. HO-2 is present abundantly in the brain and testis as a constitutive enzyme. HO-3 has been identified in brain, heart, kidney, liver, testis, and spleen. 1 Studies have suggested that CO arising from heme through metabolism by HO stimulates soluble guanylate cyclase (sGC) activity and promotes an increase in cGMP in neural and cardiovascular tissues. [2][3][4] These results implicate the HO/CO system as a potential regulator of various neural and cardiovascular functions.HO is widely expressed in the brain and is responsible for the CO-generating ability of the brain, including brain stem. 2,5 In the central nervous system (CNS), the nucleus of the solitary tract (NTS) is the site where afferent fibers arising from arterial baroreceptor, chemoreceptors, cardiopulmonary receptors, and other visceral receptors form the first central synapses 6 and thus play an important role in the integration of autonomic control of the cardiovascul...

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confidence: 88%

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confidence: 99%

Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Lin

Hsiao

et al. 2003

Hypertension

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“…CO appears to block vascular SMC growth by increasing the intracellular levels of guanosine 3 0 -5 0 -cyclic monophosphate (cGMP). CO activates both crude and purified preparations of soluble guanylate cyclase and elevates cGMP levels in vascular SMCs (Ramos et al, 1989;Brune et al, 1990;Stone and Marletta, 1994;Christodoulides et al, 1995;. Furthermore, inhibition of soluble guanylate cyclase by ODQ blocks the rise in cGMP and the antiproliferative action of HO-1 (Duckers et al, 2001).…”

Section: Ho-1 and Cell Proliferationmentioning

confidence: 99%

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

Durante

2003

Journal Cellular Physiology

143

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Heme oxygenase-1 (HO-1) catalyzes the degradation of heme to carbon monoxide (CO), iron, and biliverdin. Biliverdin is subsequently metabolized to bilirubin by the enzyme biliverdin reductase. Although interest in HO-1 originally centered on its heme-degrading function, recent findings indicate that HO-1 exerts other biologically important actions. Emerging evidence suggests that HO-1 plays a critical role in growth regulation. Deletion of the HO-1 gene or inhibition of HO-1 activity results in growth retardation and impaired fetal development, whereas HO-1 overexpression increases body size. Although the mechanisms responsible for the growth promoting properties of HO-1 are not well established, HO-1 can indirectly influence growth by regulating the synthesis of growth factors and by modulating the delivery of oxygen or nutrients to specific target tissues. In addition, HO-1 exerts important effects on critical determinants of tissue size, including cell proliferation, apoptosis, and hypertrophy. However, the actions of HO-1 are highly variable and may reflect a role for HO-1 in maintaining tissue homeostasis. Considerable evidence supports a crucial role for HO-1 in blocking the growth of vascular smooth muscle cells (SMCs). This antiproliferative effect of HO-1 is mediated primarily via the release of CO, which inhibits vascular SMC growth via multiple pathways. Pharmacologic or genetic approaches targeting HO-1 or CO to the blood vessel wall may represent a promising, novel therapeutic approach in treating vascular proliferative disorders.

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“…The activation of GC-S by CO in vitro [64] and in isolated cells [65,66] has effects similar to NO, i.e. inhibition of platelet aggregation [65] and vascular smooth muscle relaxation [67], and is accompanied by increases in intraceliular CAMP.…”

Section: Carbon Monoxidementioning

confidence: 99%

NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors

Schmidt

1992

FEBS Letters

190

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Several low molecular weight compounds are capable of activating soluble guanylyl cyclase. Recent evidence suggests that some of these are formed under physiological conditions: the nitric oxide radical, carbon monoxide and the hydroxyl radical. Thus, multiple signal transduction pathways appear to exist that form a family of guanylyl cyclase activating faclors and thereby regulate the intracellular cyclic guanosine 3',5'-monophosphatc Ievcl.

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Modulation of cyclic guanosine monophosphate levels in cultured aortic smooth muscle cells by carbon monoxide

Cited by 131 publications

References 25 publications

Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors

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Modulation of cyclic guanosine monophosphate levels in cultured aortic smooth muscle cells by carbon monoxide

Cited by 131 publications

References 25 publications

Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Interaction of Carbon Monoxide and Adenosine in the Nucleus Tractus Solitarii of Rats

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

NO•, CO and •OH Endogenous soluble guanylyl cyclase‐activating factors

Contact Info

Product

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NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors