1 Kearney P M, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet, 2005, 365: 217-223
[2]
2 Dzielak D J. The immune system and hypertension. Hypertension, 1992, 19: I36-I44
[3]
3 Fu M L. Do immune system changes have a role in hypertension? J Hypertens, 1995, 13: 1259-1265
[4]
4 Fu M L, Herlitz H, Wallukat G, et al. Functional autoimmune epitope on alpha1-adrenergic receptors in patients with malignant hypertension. Lancet, 1994, 344: 1660-1663
[5]
5 Luther H P, Homuth V, Wallukat G. Alpha1-adrenergic receptor antibodies in patients with primary hypertension. Hypertension, 1997, 29: 678-682
[6]
6 Wenzel K, Haase H, Wallukat G, et al. Potential relevance of a1-adrenergic receptor autoantibodies in refractory hypertension. PLoS One, 2008, 3: e3742
[7]
7 Yan L, Xu Y, Yao H, et al. The effects of autoantibodies against the second extracellular loop of alpha1-adrenoceptor on vasoconstriction. Basic Res Cardiol, 2009, 104: 581-589
[8]
8 Ibarra M, López-Guerrero J J, Mejía-Zepeda R, et al. Endothelium-dependent inhibition of the contractile response is decreased in aorta from aged and spontaneously hypertensive rats. Arch Med Res, 2006, 37: 334-341
[9]
9 Linder L, Kiowski W, Bühler F R, et al. Indirect evidence for release of endothelium-derived relaxing factor in human forearm circulation in vivo: blunted response in essential hypertension. Circulation, 1990, 81: 1762-1767
[10]
40 Rees D D, Cellek S, Palmer R M, et al. Dexamethasone prevents the induction by endotoxin of a nitric oxide synthase and the associated effects on vascular tone: an insight into endotoxin shock. Biochem Biophys Res Commun, 1990, 173: 541-547
[11]
41 Alonso M J, Rodríguez-Martínez M A, Martínez-Orgado J, et al. The L-arginine inhibition of rat middle cerebral artery contractile responses is mediated by inducible nitric oxide synthase. J Auton Pharmacol, 1998, 18: 105-113
[12]
10 Panza J A, García C E, Kilcoyne C M, et al. Impaired endothelium-dependent vasodilation in patients with essential hypertension. Evidence that nitric oxide abnormality is not localized to a single signal transduction pathway. Circulation, 1995, 91: 1732-1738
[13]
11 Panza J A, Quyyumi A A, Brush J E Jr, et al. Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension. New Engl J Med, 1990, 323: 22-27
[14]
12 Guimar?es S, Moura D. Vascular adrenoceptors: an update. Pharmacol Rev, 2001, 53: 319-356
[15]
13 Li J, Cao Y X, Liu H, et al. Enhanced G-protein coupled receptors-mediated contraction and reduced endothelium-dependent relaxation in hypertension. Eur J Pharmacol, 2007, 28: 186-194
[16]
14 Behrendt D, Ganz P. Endothelial function: from vascular biology to clinical applications. Am J Cardiol, 2002, 90: L40-L48
[17]
15 Luscher T F, Boulanger G M, Yang Z, et al. Interactions between endothelium derived relaxing and contracting factors in health and cardiovascular disease. Circulation, 1993, 87: S36-S44
[18]
16 Moncada S, Palmer R M, Higgs E A. Nitric oxide: physiology, pathophysiology and pharmacology. Pharmacol Rev, 1991, 43: 109-142
[19]
17 Bullock G R, Taylor S G, Weston A H. Influence of the vascular endothelium on agonist-induced contractions and relaxations in rat aorta. Brit J Pharmacol, 1986, 89: 819-830
[20]
18 Criscione L, Müller K, Forney Prescott M. Endothelial cell loss enhances the pressor response in resistance vessels. J Hypertens, 1984, 2: S441-S444
[21]
19 Eglème C, Godfraind T, Miller R C. Enhanced responsiveness of rat isolated aorta to clonidine after removal of the endothelial cell. Brit J Pharmacol, 1984, 81: 16-18
[22]
20 Martin W, Furchgott R F, Villani G M, et al. Depression of contractile responses in rat aorta by spontaneously released endothelium- derived relaxing factor. J Pharmacol Exp Ther, 1986, 237: 529-538
[23]
21 Yamaguchi T, Rodman D, O''Brien R, et al. Modulation of pulmonary artery contraction by endothelium-derived relaxing factor. Eur J Pharmacol, 1989, 161: 259-262
[24]
22 Alvarez Y, Briones A M, Hernanz R, et al. Role of NADPH oxidase and iNOS in vasoconstrictor responses of vessels from hypertensive and normotensive rats. Brit J Pharmacol, 2008, 153: 926-935
[25]
23 Félétou M, Vanhoutte P M. Endothelial dysfunction: a multifaceted disorder. Am J Physiol Heart Circ Physiol, 2006, 291: H985-H1002
[26]
24 F?rstermann U, Closs E I, Pollock J S, et al. Nitric oxide synthase isozymes. Characterization, purification, molecular cloning, and functions. Hypertension, 1994, 23: 1121-1131
[27]
25 Ridnour L A, Thomas D D, Mancardi D, et al. The chemistry of nitrosative stress induced by nitric oxide and reactive nitrogen oxide species. Putting perspective on stressful biological situations. Biol Chem, 2004, 385: 1-10
[28]
26 Upmacis R K, Crabtree M J, Deeb R S, et al. Profound biopterin oxidation and protein tyrosine nitration in tissues of ApoE-null mice on an atherogenic diet: contribution of inducible nitric oxide synthase. Am J Physiol Heart Circ Physiol, 2007, 293: H2878-H2887
[29]
27 F?rstermann U, Li H. Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling. Brit J Pharmacol, 2011, 164: 213-223
[30]
28 Liu H R, Zhao R R, Zhi J M, et al. Screening of serum autoantibodies to cardiac b1-adrenoceptors and M2-muscarinic acetylcholine receptors in 408 healthy subjects of varying ages. Autoimmunity, 1999, 29: 43-51
[31]
29 Porstmann T, Kiessig S T. Enzyme immunoassay techniques-an overview. J Immunol Methods, 1992, 150: 5-21
[32]
30 Tao L, Liu H R, Gao F, et al. Mechanical traumatic injury without circulatory shock causes cardiomyocyte apoptosis: role of reactive nitrogen and reactive oxygen species. Am J Physiol Heart Circ Physiol, 2005, 288: H2811-H2818
[33]
31 Alvarez Y, Briones A M, Balfagón G, et al. Hypertension increases the participation of vasoconstrictor prostanoids from cyclo- oxygenase-2 in phenylephrine responses. J Hypertens, 2005, 23: 767-777
[34]
32 Alvarez Y, Pérez-Girón J V, Hernanz R, et al. Losartan reduces the increased participation of COX-2 derived products in vascular responses of hypertensive rats. J Pharmacol Exp Ther, 2007, 321: 381-388
[35]
33 Fu M L, Wallukat G, Hjalmarson A, et al. Characterization of anti-peptide antibodies directed against an extracellular immunogenic epitope on the human a1-adrenergic receptor. Clin Exp Immunol, 1994, 97: 146-151
[36]
34 Bkaily G, El-Bizri N, Bui M, et al. Modulation of intracellular Ca2+ via L-type calcium channels in heart cells by the autoantibody directed against the second extracellular loop of the alpha1-adrenoceptors. Can J Physiol Pharmacol, 2003, 81: 234-246
[37]
35 Dora K A, Hinton J M, Walker S D, et al. An indirect influence of phenylephrine on the release of endothelium-derived vasodilators in rat small mesenteric artery. Brit J Pharmacol, 2000, 129: 381-387
[38]
36 Nishina H, Ozaki T, Hanson M A, et al. Mechanism of noradrenaline-induced vasorelaxation in isolated femoral arteries of the neonatal rat. Brit J Pharmacol, 1999, 127: 809-812
[39]
37 Mendez E, Calzada C, Ocharan E, et al. Differential expression of alpha1-adrenergic receptor subtypes in coronary microvascular endothelial cells in culture. Eur J Pharmacol, 2006, 546: 127-133
[40]
38 Briones A M, Alonso M J, Hernanz R, et al. Alterations of the nitric oxide pathway in cerebral arteries from spontaneously hypertensive rats. J Cardiovasc Pharmacol, 2002, 39: 378-388
[41]
39 Vaziri N D, Ni Z, Oveisi F. Upregulation of renal and vascular nitric oxide synthase in young spontaneously hypertensive rats. Hypertension, 1998, 31: 1248-1254