In Vivo Evidence for Nitric Oxide–Mediated Calcium-Activated Potassium-Channel Activation During Human Endotoxemia
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[1] M. Singer,et al. Reversal of life-threatening, drug-related potassium-channel syndrome by glibenclamide , 2005, The Lancet.
[2] L. Kelly,et al. Effect of Potassium Channel and Cytochrome P450 Inhibition on Transient Hypotension and Survival during Lipopolysaccharide-Induced Endotoxic Shock in the Rat , 2005, Pharmacology.
[3] M. Singer,et al. The pore‐forming subunit of the KATP channel is an important molecular target for LPS‐induced vascular hyporeactivity in vitro , 2005, British journal of pharmacology.
[4] J. G. van der Hoeven,et al. ACTIVATION OF THE ATP-DEPENDENT POTASSIUM CHANNEL ATTENUATES NOREPINEPHRINE-INDUCED VASOCONSTRICTION IN THE HUMAN FOREARM , 2004, Shock.
[5] D. Webb,et al. Comparison of two plethysmography systems in assessment of forearm blood flow. , 2004, Journal of applied physiology.
[6] J. Bakker,et al. Administration of the nitric oxide synthase inhibitor NG-methyl-l-arginine hydrochloride (546C88) by intravenous infusion for up to 72 hours can promote the resolution of shock in patients with severe sepsis: Results of a randomized, double-blind, placebo-controlled multicenter study (study no. 144- , 2004, Critical care medicine.
[7] J. Bakker,et al. Multiple-center, randomized, placebo-controlled, double-blind study of the nitric oxide synthase inhibitor 546C88: Effect on survival in patients with septic shock* , 2004, Critical care medicine.
[8] M. Wolzt,et al. Inflammation-induced vasoconstrictor hyporeactivity is caused by oxidative stress. , 2003, Journal of the American College of Cardiology.
[9] M. Joyner,et al. Blunted Sympathetic Vasoconstriction in Contracting Skeletal Muscle of Healthy Humans: is Nitric Oxide Obligatory? , 2003, The Journal of physiology.
[10] Pritpal S Tamber,et al. The Surviving Sepsis Campaign: raising awareness to reduce mortality , 2003, Critical care.
[11] M. Netea,et al. TNFα AND IL-1β EXERT NO DIRECT VASOACTIVITY IN HUMAN ISOLATED RESISTANCE ARTERIES , 2002 .
[12] T. B. Paiva,et al. Different mechanism of LPS‐induced vasodilation in resistance and conductance arteries from SHR and normotensive rats , 2002, British journal of pharmacology.
[13] U. Prabhakar,et al. Simultaneous quantification of proinflammatory cytokines in human plasma using the LabMAP assay. , 2002, Journal of immunological methods.
[14] J. Assreuy,et al. Differential Involvement of Guanylate Cyclase and Potassium Channels in Nitric Oxide-Induced Hyporesponsiveness to Phenylephrine in Endotoxemic Rats , 2002, Shock.
[15] M. Wolzt,et al. Adrenoceptor Hyporeactivity Is Responsible for Escherichia coli Endotoxin‐Induced Acute Vascular Dysfunction in Humans , 2002, Arteriosclerosis, thrombosis, and vascular biology.
[16] M. Netea,et al. TNFalpha and IL-1beta exert no direct vasoactivity in human isolated resistance arteries. , 2002, Cytokine.
[17] J. Eldstrom,et al. Lipopolysaccharide can activate BK channels of arterial smooth muscle in the absence of iNOS expression. , 2001, Biochimica et biophysica acta.
[18] D. Landry,et al. The pathogenesis of vasodilatory shock. , 2001, The New England journal of medicine.
[19] G. Clermont,et al. Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care , 2001, Critical care medicine.
[20] Alun D. Hughes,et al. In vivo evidence for KCa channel opening properties of acetazolamide in the human vasculature , 2001, British journal of pharmacology.
[21] S. Yang,et al. Hyperpolarization contributes to vascular hyporeactivity in rats with lipopolysaccharide-induced endotoxic shock. , 2000, Life sciences.
[22] I. Gartside,et al. Description and validation of a novel liquid metal-free device for venous congestion plethysmography. , 2000, Journal of applied physiology.
[23] M. Yen,et al. Abnormal activation of K+ channels in aortic smooth muscle of rats with endotoxic shock: electrophysiological and functional evidence , 2000, British journal of pharmacology.
[24] J. Assreuy,et al. Involvement of soluble guanylate cyclase and calcium-activated potassium channels in the long-lasting hyporesponsiveness to phenylephrine induced by nitric oxide in rat aorta , 2000, Naunyn-Schmiedeberg's Archives of Pharmacology.
[25] D. Annane,et al. Compartmentalised inducible nitric-oxide synthase activity in septic shock , 2000, The Lancet.
[26] M. Yen,et al. Role of nitric oxide and K+-channels in vascular hyporeactivity induced by endotoxin , 1999, Naunyn-Schmiedeberg's Archives of Pharmacology.
[27] L S Murray,et al. How reproducible is bilateral forearm plethysmography? , 1998, British journal of clinical pharmacology.
[28] L. Clapp,et al. Abnormal activation of K+ channels underlies relaxation to bacterial lipopolysaccharide in rat aorta. , 1996, Biochemical and biophysical research communications.
[29] C. Szabó,et al. Inhibition of ATP-activated potassium channels exerts pressor effects and improves survival in a rat model of severe hemorrhagic shock. , 1996, Shock.
[30] G. Vanelli,et al. Glibenclamide, a blocker of ATP‐sensitive potassium channels, reverses endotoxin‐induced hypotension in pig , 1995, Experimental physiology.
[31] S. Archer,et al. Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[32] R. Cohen,et al. Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle , 1994, Nature.
[33] D. Landry,et al. The ATP-sensitive K+ channel mediates hypotension in endotoxemia and hypoxic lactic acidosis in dog. , 1992, The Journal of clinical investigation.
[34] J. Kovacs,et al. The cardiovascular response of normal humans to the administration of endotoxin. , 1989, The New England journal of medicine.
[35] J E Parrillo,et al. Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. , 1987, Critical care medicine.
[36] Timmermans Pb,et al. Postsynaptic alpha 1- and alpha 2-adrenoceptor blocking properties of (dihydro)quinidine and (dihydro)quinine. , 1983 .
[37] P. Timmermans,et al. Postsynaptic alpha 1- and alpha 2-adrenoceptor blocking properties of (dihydro)quinidine and (dihydro)quinine. , 1983, Arzneimittel-Forschung.
[38] S. Hoobler,et al. STUDIES ON VASOMOTOR TONE. I. THE EFFECT OF THE TETRA-ETHYLAMMONIUM ION ON THE PERIPHERAL BLOOD FLOW OF NORMAL SUBJECTS. , 1949, The Journal of clinical investigation.
[39] K. Campbell,et al. The use of tetraethylammonium in peripheral vascular disease and causalgic states; a new method for producing blockade of the autonomic ganglion. , 1947, Surgery.
[40] Campbell Kn,et al. The use of tetraethylammonium in peripheral vascular disease and causalgic states; a new method for producing blockade of the autonomic ganglion. , 1946 .