Changing standard chow diet promotes vascular NOS dysfunction in Dahl S rats.
暂无分享,去创建一个
J. Pollock | D. Pollock | D. Ho | F. Spradley | K. Kang
[1] D. Mattson,et al. High Dietary Protein Exacerbates Hypertension and Renal Damage in Dahl SS Rats by Increasing Infiltrating Immune Cells in the Kidney , 2011, Hypertension.
[2] J. Falck,et al. Modulation by Cytochrome P450‐4A ω‐Hydroxylase Enzymes of Adrenergic Vasoconstriction and Response to Reduced PO2 in Mesenteric Resistance Arteries of Dahl Salt‐Sensitive Rats , 2010, Microcirculation.
[3] D. Atochin,et al. Endothelial nitric oxide synthase transgenic models of endothelial dysfunction , 2010, Pflügers Archiv - European Journal of Physiology.
[4] Paul L Huang,et al. The Akt1-eNOS Axis Illustrates the Specificity of Kinase-Substrate Relationships in Vivo , 2009, Science Signaling.
[5] J. Pollock,et al. PP2B-dependent NO production in the medullary thick ascending limb during diabetes. , 2009, American journal of physiology. Renal physiology.
[6] T. Fujita,et al. Protective Effect of Dietary Potassium Against Vascular Injury in Salt-Sensitive Hypertension , 2008, Hypertension.
[7] J. Pollock,et al. Novel Nitric Oxide Synthase–Dependent Mechanism of Vasorelaxation in Small Arteries From Hypertensive Rats , 2007, Hypertension.
[8] J. Pollock,et al. In vivo evidence for endothelin-1-mediated attenuation of alpha1-adrenergic stimulation. , 2006, American journal of physiology. Heart and circulatory physiology.
[9] Kakoli Parai,et al. Effects of Chloride Substitution in Isolated Mesenteric Blood Vessels from Dahl Normotensive and Hypertensive Rats , 2005, Journal of cardiovascular pharmacology.
[10] Kakoli Parai,et al. Impact of Nitric Oxide Synthase Inhibitor and Chloride Channel Antagonist on Mesenteric Vascular Conductance in Anesthetized Dahl Normotensive and Hypertensive Rats , 2005, Journal of cardiovascular pharmacology.
[11] W. Durante,et al. Arginase inhibition restores arteriolar endothelial function in Dahl rats with salt-induced hypertension. , 2005, American journal of physiology. Regulatory, integrative and comparative physiology.
[12] S. Moncada,et al. Investigation of Vascular Responses in Endothelial Nitric Oxide Synthase/Cyclooxygenase-1 Double-Knockout Mice: Key Role for Endothelium-Derived Hyperpolarizing Factor in the Regulation of Blood Pressure in Vivo , 2005, Circulation.
[13] J. Pollock,et al. NADPH Oxidase Inhibition Attenuates Oxidative Stress but Not Hypertension Produced by Chronic ET-1 , 2005, Hypertension.
[14] H. Jacob,et al. Genome-wide scanning with SSLPs in the rat. , 2005, Methods in molecular medicine.
[15] K. Homma,et al. Impaired nitric oxide‐ and endothelium‐derived hyperpolarizing factor‐dependent dilation of renal afferent arteriole in Dahl salt‐sensitive rats , 2004, Nephrology.
[16] E. Jaimes,et al. Atorvastatin Prevents End-Organ Injury in Salt-Sensitive Hypertension: Role of eNOS and Oxidant Stress , 2004, Hypertension.
[17] Andrew S Greene,et al. Influence of diet and genetics on hypertension and renal disease in Dahl salt-sensitive rats. , 2004, Physiological genomics.
[18] S. Black,et al. Emergence of Smooth Muscle Cell Endothelin B–Mediated Vasoconstriction in Lambs With Experimental Congenital Heart Disease and Increased Pulmonary Blood Flow , 2003, Circulation.
[19] J. Lombard,et al. Skeletal Muscle Arteriolar Reactivity in SS.BN13 Consomic Rats and Dahl Salt-Sensitive Rats , 2003, Hypertension.
[20] W. Durante,et al. Heme Oxygenase Inhibitor Restores Arteriolar Nitric Oxide Function in Dahl Rats , 2003, Hypertension.
[21] M. Boegehold. Microvascular Structure and Function in Salt‐Sensitive Hypertension , 2002, Microcirculation.
[22] M. Weinberger. Salt Sensitivity Is Associated With an Increased Mortality in Both Normal and Hypertensive Humans , 2002, Journal of clinical hypertension.
[23] G. Werner-Felmayer,et al. Nitric-oxide-mediated relaxations in salt-induced hypertension: effect of chronic β1-selective receptor blockade , 2002, Journal of hypertension.
[24] J. A. Duggan,et al. Effect of nitric oxide synthase inhibitor N(omega) nitro-L-arginine methyl ester on relaxant responses to calcium channel antagonists in isolated aortic rings from Dahl normotensive and hypertensive rats. , 2002, Journal of cardiovascular pharmacology.
[25] T. Meinertz,et al. Endothelial Dysfunction, Oxidative Stress, and Risk of Cardiovascular Events in Patients With Coronary Artery Disease , 2001, Circulation.
[26] P. Vallance,et al. An Endothelium-Derived Hyperpolarizing Factor–Like Factor Moderates Myogenic Constriction of Mesenteric Resistance Arteries in the Absence of Endothelial Nitric Oxide Synthase–Derived Nitric Oxide , 2001, Hypertension.
[27] T. Lüscher,et al. Vasopeptidase Inhibition Exhibits Endothelial Protection in Salt-Induced Hypertension , 2001, Hypertension.
[28] N. Fineberg,et al. Salt Sensitivity, Pulse Pressure, and Death in Normal and Hypertensive Humans , 2001, Hypertension.
[29] J. A. Duggan,et al. The interrelationship between chloride ions and endothelium on alpha(1)-adrenoceptor-mediated contractions in aortic rings from Dahl normotensive and hypertensive rats. , 2000, Cardiovascular research.
[30] P. Huang,et al. An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[31] T. Lüscher,et al. Dysfunctional renal nitric oxide synthase as a determinant of salt-sensitive hypertension: mechanisms of renal artery endothelial dysfunction and role of endothelin for vascular hypertrophy and Glomerulosclerosis. , 2000, Journal of the American Society of Nephrology : JASN.
[32] N. Vaziri,et al. Nitric oxide synthase isotype expression in salt-sensitive and salt-resistant Dahl rats. , 1999, Hypertension.
[33] L. Raij,et al. Relationship between hypercholesterolaemia, endothelial dysfunction and hypertension. , 1999, Journal of hypertension.
[34] J. M. Doughty,et al. Charybdotoxin and apamin block EDHF in rat mesenteric artery if selectively applied to the endothelium. , 1999, The American journal of physiology.
[35] H. Kosaka,et al. Role of nitric oxide in vascular hyper‐responsiveness to norepinephrine in hypertensive Dahl rats , 1998, Journal of hypertension.
[36] S. Davidge. Oxidative Stress and Altered Endothelial Cell Function in Preeclampsia , 1998, Seminars in reproductive endocrinology.
[37] L. Raij,et al. Endothelial dysfunction and cardiorenal injury in experimental salt-sensitive hypertension: effects of antihypertensive therapy. , 1997, Circulation.
[38] N. Hirawa,et al. Restoration of endothelial cell function by chronic cicletanine treatment in Dahl salt-sensitive rats with salt-induced hypertension. , 1996, Hypertension research : official journal of the Japanese Society of Hypertension.
[39] T. Lüscher,et al. L-NAME hypertension alters endothelial and smooth muscle function in rat aorta. Prevention by trandolapril and verapamil. , 1995, Hypertension.
[40] P. Vanhoutte,et al. Chronic treatment with the CA2+ channel inhibitor RO 40-5967 potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive Dahl rat. , 1994, Blood pressure.
[41] Boegehold Ma,et al. Microvascular responses to oxygen and muscle contraction in hypertensive Dahl rats. , 1993 .
[42] M. Boegehold. Enhanced arteriolar vasomotion in rats with chronic salt-induced hypertension. , 1993, Microvascular research.
[43] C. Vrints,et al. Paradoxical vasoconstriction as result of acetylcholine and serotonin in diseased human coronary arteries. , 1992, European heart journal.
[44] P. Ganz,et al. Patients With Evidence of Coronary Endothelial Dysfunction as Assessed by Acetylcholine Infusion Demonstrate Marked Increase in Sensitivit to Constrictor Effects of Catecholamines , 1992, Circulation.
[45] M. Boegehold. Reduced influence of nitric oxide on arteriolar tone in hypertensive Dahl rats. , 1992, Hypertension.
[46] D. L. Maude,et al. Salt Excretion and Vascular Resistance of Perfused Kidneys of Dahl Rats , 1982, Hypertension.