Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein.

Ignarro, Louis J.

doi:10.1161/01.res.65.1.1

Cited by 898 publications

(409 citation statements)

References 168 publications

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“…Since human primary hypertension is associated with increased peripheral vascular resistance (28), there are theoretical reasons why reduced NO production or bioavailability could lead to vasoconstriction, and hence, increased peripheral vascular resistance, resulting in hypertension. Incubation of blood vessels with cadmium was reported to inhibit endothelium-dependent vasorelaxation (21), which is mainly mediated by NO from the vascular endothelium (29). However, it has not been determined whether vasorelaxation is altered in cadmium-accumulated blood vessels.…”

Section: Discussionmentioning

confidence: 99%

Effects of cadmiumin vitro on contractile and relaxant responses of isolated rat aortas

Takahashi

Poteser

Masui

et al. 2004

Environ Health Prev Med

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Objective: Cadmium is known to affect the vascular tone of isolated blood vessels in vitro and the arterial pressure of rats in vivo. However, the mechanisms of cadmium actions on the vascular system have not been clarified. To elucidate the actions of cadmium on vascular tonus, effects of cadmium on vasocontractile and vasorelaxant responses in vitro were investigated using aortic strips isolated from rats.Methods: Aortic strips isolated from male Wistar rats were incubated with CdCl 2 (10 μM) for 24 hr, washed with fresh CdCl 2 -free medium, and then used for measurement of isometric tension and Western blot analysis of eNOS (endothelial nitric oxide synthase) and iNOS (inducible nitric oxide synthase).Results: In the aortas pretreated with cadmium in vitro, the contractile response to phenylephrine was significantly higher than that in the control aortic strips pretreated with a vehicle. The sodium nitroprusside-induced relaxing response was significantly higher in the aortic strips pretreated with cadmium for 24 hr, compared with that in the control pretreated with a vehicle. The isoproterenolinduced relaxing response was also significantly higher in the cadmium-accumulated aortic strips. In vitro cadmium treatment slightly but not significantly increased the acetylcholine-induced relaxation of the aortic strips. Cadmium treatment induced expression of iNOS and significantly increased expression of eNOS in the aortic strips, while it did not affect expression of β-actin.Conclusions: Cadmium treatment in vitro augmented the α1 adrenoceptor-mediated contractile response, even though eNOS and iNOS were upregulated by cadmium treatment. NO-induced and β-adrenoceptor-mediated relaxing responses were also augmented by cadmium treatment. These results suggest that both vasocontractile and vasorelaxing responses are augmented in cadmiumaccumulated aortas.

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Section: Discussionmentioning

confidence: 99%

Effects of cadmiumin vitro on contractile and relaxant responses of isolated rat aortas

Takahashi

Poteser

Masui

et al. 2004

Environ Health Prev Med

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“…Nitric oxide (NO) or a related substance has been shown to be an endothelium-derived relaxing factor (Ignarro, 1989;Moncada et aI., 1991). NO, which is synthesized from the terminal guanidino nitrogen atoms of the basic amino acid L-arginine (Palmer et ai., 1988) by NO synthases (Bredt and Snyder, 1990;Stuehr et al, 1991), induces vasodilation via activation of soluble guanylate cyclase (Ignarro, 1989;Moncada et aI., 1991).…”

mentioning

confidence: 99%

“…NO, which is synthesized from the terminal guanidino nitrogen atoms of the basic amino acid L-arginine (Palmer et ai., 1988) by NO synthases (Bredt and Snyder, 1990;Stuehr et al, 1991), induces vasodilation via activation of soluble guanylate cyclase (Ignarro, 1989;Moncada et aI., 1991). Accordingly, an over production of NO resulting from induction of an inducible NO synthase in endothelial and smooth muscle cells by endotoxin, and therefore a decrease in vascular reactivity, have been implicated in sep tic shock following bacterial infection (Knowles et aI., 1990;Radomski et aI., 1990;Salvemini et aI., 1990Salvemini et aI., , 1992.…”

mentioning

confidence: 99%

Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

Ueno

Lee

1993

J Cereb Blood Flow Metab

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Summary: The effects of endotoxin (lipopolysaccharide; LPS) on the reactivity of isolated porcine basilar artery were examined using in vitro tissue bath techniques. The active muscle tone of the basilar arterial rings with or without endothelial cells induced by U46619 (1 fl-M) reached a plateau in 15 min, which was stable for the first hour and gradually decreased during the next 5 h. This time-dependent decrease in tone was significantly poten tiated in the presence of LPS (20 fl-g/ml). Gram-negative bacteria are pathogens commonly involved in infections of the CNS (Tunkel and Scheld, 1991) and in endotoxic shock, which is characterized by hypotension, vascular injury, and resistance to vasoconstrictors in various species (Miller et aI., 1987; Van Deventer et aI., 1988; Suf fredini et aI., 1989; Auguet et ai., 1991; Dal N ogare, 1991). A marked decrease in CBF resulting from hypotension following exposure to endotoxin has been reported (Miller et aI., 1987; N ishijima et ai., 1988). The exact mechanisms responsible for endo toxin-induced hypotension and the decrease in CBF remain unclear.Endotoxin (lipopolysaccharide; LPS), which is the toxic moiety of the gram-negative bacterial outer membrane, has been shown to induce vascu- 712U46619 and KCI were decreased following incubation with LPS (20 fl-g/ml) for 4 h. Similar hyporeactivity was observed in cold storage-denervated cerebral arteries in cubated with LPS for 4 h. This decrease in contractile responses in LPS-treated rings was reversed by 60 fl-M L-NNA and 1 fl-M dexamethasone. These results indicate that LPS treatment renders the porcine basilar arteries hyporesponsive to vasoconstrictors. Since effects of LPS were not modified by the presence of endothelial cells and perivascular neurons, the alteration in cerebral arterial reactivity may be due in part to an enhanced formation of nitric oxide from L-arginine in the vascular smooth mus cle cells.

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“…Nitric oxide has a very short half-life (2 to 5 s), making it easy to administer into the lungs. 6 Early experiments in animals showed that iNO produced acute and sustained vasodilatation when given via inhalation. 7 These initial results led to pilot trials in babies showing that, when iNO was administered in severe pulmonary hypertension, an improvement in oxygenation was seen.…”

Section: Introductionmentioning

confidence: 99%

Inhaled nitric oxide in term and preterm infants

Sekar

2006

J Perinatol

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Nitric oxide (NO) is a gas that has potent vasodilator properties. It can be administered via inhalation in situations where NO production is impaired and results in vasodilatation of the pulmonary capillaries. In term infants, the administration of inhaled NO, at a dose of 20 parts per million, may reduce the need for extracorporeal membrane oxygenation by reducing pulmonary vascular resistance and improving oxygenation. Inhaled NO is an approved therapy in term babies with severe hypoxemic respiratory failure. In premature infants, inhaled NO may increase bleeding time and decrease platelet aggregation resulting in an increased risk for intraventricular hemorrhage. Early administration of inhaled NO may also potentially decrease the risk for developing chronic lung disease in premature infants. However, since studies show conflicting results, inhaled NO should only be used in premature neonates following investigational review board approved protocols.

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Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein.

Cited by 898 publications

References 168 publications

Effects of cadmiumin vitro on contractile and relaxant responses of isolated rat aortas

Effects of cadmiumin vitro on contractile and relaxant responses of isolated rat aortas

Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

Inhaled nitric oxide in term and preterm infants

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