ライフサイエンスコーパス: essential hypertension

1 ic basis for clinical heterogeneity of human essential hypertension.

2 ering and treatment modality in persons with essential hypertension.

3 ypertension trial, and a 31-patient trial in essential hypertension.

4 chological stress are at risk for developing essential hypertension.

5 he human genome for susceptibility genes for essential hypertension.

6 ory care visits as cardiovascular disease or essential hypertension.

7 is a key contributor to the pathogenesis of essential hypertension.

8 aminergic action in genetic rodent and human essential hypertension.

9 ic deprivation, maternal height and age, and essential hypertension.

10 endothelin was measured in 47 patients with essential hypertension.

11 terial pressure of patients with established essential hypertension.

12 s in part for individual susceptibilities to essential hypertension.

13 e to improve blood pressure in patients with essential hypertension.

14 nce our understanding of the pathogenesis of essential hypertension.

15 n in Caucasians, but was not associated with essential hypertension.

16 olated systolic hypertension from those with essential hypertension.

17 is may be underlying variability in types of essential hypertension.

18 er, and this gene locus is linked with human essential hypertension.

19 ted the genetic dissection of more prevalent essential hypertension.

20 neously hypertensive (SH) rat model of human essential hypertension.

21 ication of major genes contributing to human essential hypertension.

22 relatively prevalent in young patients with essential hypertension.

23 LV geometry in children and adolescents with essential hypertension.

24 humans and, in particular, in subjects with essential hypertension.

25 derived from results among the subjects with essential hypertension.

26 mature cardiovascular death in patients with essential hypertension.

27 us region on human chromosome 17 in familial essential hypertension.

28 l Na-Li exchange in diabetic nephropathy and essential hypertension.

29 latelets and lymphocytes) from patients with essential hypertension.

30 long-term basis in the SH rat model of human essential hypertension.

31 e related directly to the pathophysiology of essential hypertension.

32 the long-term consequences of uncomplicated essential hypertension.

33 hich has been implicated in the mechanism of essential hypertension.

34 one of the polymorphisms was associated with essential hypertension.

35 , and above all, preventive measures against essential hypertension.

36 of both single nucleotide polymorphisms with essential hypertension.

37 characteristics with those of uncomplicated essential hypertension.

38 herapeutic implications in the management of essential hypertension.

39 nt a novel mechanism for the pathogenesis of essential hypertension.

40 ng with apnoea, congestive heart failure and essential hypertension.

41 astolic BP to assess their overall impact on essential hypertension.

42 ypoxia were higher in untreated ARAS than in essential hypertension.

43 associated with high sympathetic outflow in essential hypertension.

44 in the regulation of sympathetic activity in essential hypertension.

45 onduit artery endothelial dysfunction during essential hypertension.

46 ood pressure control, than for patients with essential hypertension.

47 to conduit artery endothelial dysfunction in essential hypertension.

48 min C modifies sympathetic nerve activity in essential hypertension.

49 re homeostasis and the pathogenesis of human essential hypertension.

50 h MR antagonists compared with patients with essential hypertension.

51 N and elevated sympathetic vasomotor tone in essential hypertension.

52 crease in blood pressure in individuals with essential hypertension.

53 creased blood pressure in most patients with essential hypertension.

54 en (AGT) gene locus is associated with human essential hypertension.

55 on are a potential causative risk factor for essential hypertension.

56 tension and is commonly present in new-onset essential hypertension.

57 ve insulin resistance in human subjects with essential hypertension.

58 g early kidney damage in the pathogenesis of essential hypertension.

59 eliorate insulin resistance in subjects with essential hypertension.

60 ls, T cells, and salt in the pathogenesis of essential hypertension.

61 stematic two-dimensional (2D) genome-scan of essential hypertension.

62 pressure lowering and treatment modality in essential hypertension.

63 tributes to the heritable component of human essential hypertension.

64 is of experimental volume-expanded and human essential hypertension.

65 or 65% to 75% of the risk for human primary (essential) hypertension.

66 gher major cardiovascular events (MACE) than essential hypertension (23.3% vs 19.3%, p = 0.015).

67 Essential hypertension (31.4%, 39.3%, and 76.2%, respect

68 nism on MR antagonists than in patients with essential hypertension (56.3 [95% CI 48.8-64.7] vs 26.6

69 Essential hypertension, a common complex disease, displa

70 ne chromogranin A (CHGA) is overexpressed in essential hypertension, a complex trait with genetic pre

71 In nondiabetic individuals with essential hypertension, a group known to be insulin resi

72 n criteria for this study were: diagnosis of essential hypertension, absence of renal failure, and do

73 Essential hypertension affects 1 billion people worldwid

74 ere determined in 28 untreated patients with essential hypertension and 30 normotensive control subje

75 In patients with essential hypertension and baseline electrocardiographic

76 Essential hypertension and cardiovascular-renal-target o

77 identified patients aged 55 to 80 years with essential hypertension and electrocardiographic LV hyper

78 Both human essential hypertension and genetically induced hypertens

79 diverse population of 303 men and women with essential hypertension and increased LV mass at screenin

80 ipants aged 25 to 75 years with uncontrolled essential hypertension and Internet access.

81 (LVH[-]) were compared with 25 patients with essential hypertension and left ventricular hypertrophy

82 A total of 960 patients with essential hypertension and LV hypertrophy (LVH) on scree

83 utative link between it and mild to moderate essential hypertension and nephrosclerosis; angiotensin-

84 indicate that white subjects with moderate, essential hypertension and normal kidney function have n

85 ification of the genetic influences on human essential hypertension and other complex diseases has pr

86 o had newly diagnosed, never-treated stage 1 essential hypertension and serum uric acid levels > or =

87 Y1 as a potential candidate gene involved in essential hypertension and the cardiometabolic syndrome.

88 phenotypes) to identify candidate genes for essential hypertension and the metabolic syndrome.

89 izing hypothesis on the role of uric acid in essential hypertension and the practical application of

90 disorders has been reported in patients with essential hypertension and we have described disordered

91 Despite the high prevalence of essential hypertension and years of research, the basic

92 to diabetic nephropathy and proteinuria with essential hypertension, and numerous studies have demons

93 triacylglycerol and low HDL concentrations, essential hypertension, and procoagulant and proinflamma

94 Coronary arteriosclerosis, essential hypertension, angina, and pre-infarction syndr

95 he rate of gastric emptying in patients with essential hypertension, another disease considered to be

96 ction, infections, and effect on preexisting essential hypertension are also described.

97 is consistent with evidence that ageing and essential hypertension are both associated with defects

98 the genes responsible for susceptibility to essential hypertension are mostly unknown.

99 levels and susceptibility to development of essential hypertension are partially determined by genet

100 n; however, only a minority of patients with essential hypertension are salt sensitive.

101 betes, obesity, combined hyperlipidaemia and essential hypertension, are complex disorders whose gene

102 We focus on patients with essential hypertension because this is the most prevalen

103 re then compared with those of patients with essential hypertension but without MetS for the same mea

104 d cation proton antiporter, is implicated in essential hypertension by gene linkage analysis.

105 tly NO production in patients with untreated essential hypertension by measurement of synthesis of in

106 Essential hypertension can be defined as a rise in blood

107 n subjects with recently diagnosed PA and 54 essential hypertension controls were recruited.

108 Essential hypertension, defined as elevated levels of bl

109 Because approximately 40% of patients with essential hypertension demonstrate low renin, we suggest

110 c to the heart and kidneys seems to occur as essential hypertension develops.

111 om sibships in which two or more members had essential hypertension diagnosed before age 60 yr.

112 ears; 22 men, 18 women) and 32 patients with essential hypertension (EH) (age range, 26-85 years; 19

113 ommon WNK1 variants might also contribute to essential hypertension (EH), a multifactorial disorder a

114 n to potentially contribute to prevention of essential hypertension (EH).

115 jects and a group of untreated patients with essential hypertension (EH).

116 underwent adrenalectomy and 25 patients with essential hypertension (EH).

117 mal (NT), high normal (HN), or stages 1 to 3 essential hypertension (EHT-1, EHT-2/3).

118 Family history of essential hypertension explained ethnic differences in d

119 gonists and 41 853 age-matched patients with essential hypertension from the registry.

120 y, one (n = 43) with demographically defined essential hypertension (group I) and the other (n = 60)

121 Essential hypertension has a heritability as high as 30-

122 These findings imply that human essential hypertension has an oligogenic element (a few

123 ive rat (SHR), a widely used animal model of essential hypertension, has a global defect in insulin a

124 Patients with essential hypertension have impaired endothelial NO acti

125 or loss of function, genetic determinants of essential hypertension, high blood pressure of unknown c

126 search on a link between angiotensinogen and essential hypertension illustrates a path that began in

127 rs13306560 was associated with essential hypertension in adults (odds ratio, 4.281; 95%

128 Essential hypertension in black patients also shows clin

129 could be the most common secondary cause of essential hypertension in black people identified to dat

130 The pathogenesis of essential hypertension in blacks may differ from that in

131 own an association between hyperuricemia and essential hypertension in children, presenting the possi

132 c acid level as a biomarker for diagnosis of essential hypertension in children.

133 similarly implicated in the pathogenesis of essential hypertension in Chinese by carrying out linkag

134 w insights into mechanisms for some forms of essential hypertension in humans, a disease that afflict

135 II, constitute inherited predispositions to essential hypertension in humans.

136 2 family 2 (NR2F2), as being associated with essential hypertension in humans.

137 elastin may contribute to the development of essential hypertension in patients.

138 Despite common wisdom, the role of essential hypertension in the etiopathogenesis of ESRD h

139 been reported linked to and associated with essential hypertension in White Europeans, African-Carib

140 um creatinine, renal crisis, or grade 3 or 4 essential hypertension) in 7 patients who had received r

141 e opposite in direction to those observed in essential hypertension, in which MetS is absent.

142 randomly selected patients and families with essential hypertension, inheritance involves many genes

143 Essential hypertension involves an increase in sympathet

144 Essential hypertension is a common disease, yet its path

145 Essential hypertension is a common multifactorial trait.

146 There is increasing evidence that essential hypertension is associated with a panoply of m

147 studies in younger age groups that show that essential hypertension is associated with nocturia and w

148 Essential hypertension is characterized by both increase

149 Essential hypertension is characterized by reciprocal re

150 at whole-body NO production in patients with essential hypertension is diminished under basal conditi

151 suggest that the endothelial dysfunction in essential hypertension is due to a selective abnormality

152 Essential hypertension is probably caused by combination

153 cceleration of atherosclerosis by polygenic (essential) hypertension is well-characterized in humans;

154 hypertensive rat (SHR), a genetic model for essential hypertension, is due at least partly to a cent

155 In 1999, essential hypertension, ischemic heart disease, congesti

156 small number of patients labelled as having "essential" hypertension, it is a potentially reversible

157 Despite the prevalence of essential hypertension, its underlying genetic basis has

158 e 2 diabetes mellitus, hypertriglyceridemia, essential hypertension, low circulating high-density lip

159 ur patients with uncomplicated and untreated essential hypertension (LVH[-]) were compared with 25 pa

160 e that salt-sensitivity of blood pressure in essential hypertension may result from impairment of a n

161 e subjects, one with demographically defined essential hypertension (n = 43) and the other (n = 60) w

162 cells/kg; n=6), patients with RVD (n=12) or essential hypertension (n=12), and healthy volunteers (n

163 stent revascularization, or in patients with essential hypertension (n=32), during fixed Na(+) intake

164 carotid bodies are hyperactive at rest, e.g. essential hypertension, obstructive sleep apnoea and hea

165 provided additional evidence in established essential hypertension of increased central sympathetic

166 n the basis of low risk in white donors with essential hypertension, our transplant center undertook

167 t solve the dilemma regarding the origins of essential hypertension, partly because there are many te

168 Essential hypertension probably results from combination

169 The pathogenesis of essential hypertension remains unknown, but thiazide diu

170 nhibitors versus ARBs in adult patients with essential hypertension, reported an outcome of interest,

171 Essential hypertension results from a mosaic of patholog

172 We propose that nocturnal polyuria and essential hypertension share some of the same pathophysi

173 Analysis of human subjects with essential hypertension showed 2.6-fold increase in SOD2

174 We now report that, in human essential hypertension, single nucleotide polymorphisms

175 m enhancement in PA (70%) when compared with essential hypertension subjects (13%; P<0.0001) with no

176 rong correlation between uric acid level and essential hypertension, supporting its use in diagnosis.

177 ghly abundant among a group of patients with essential hypertension that are refractory to standard t

178 ndothelial dysfunction are early features of essential hypertension that may antedate blood pressure

179 me registry, we identified a population with essential hypertension that was frequency matched by dec

180 Compared with essential hypertension, the excess risk for cardiovascul

181 inogen (AGT) gene locus is involved in human essential hypertension, the molecular mechanisms involve

182 Finally, in adolescents with new-onset essential hypertension, the prevalence of elevated serum

183 CE inhibitors on cardiovascular mortality in essential hypertension, the role of ACE inhibitors in pa

184 ble mechanism of a genetic predisposition to essential hypertension; they may also have important evo

185 0 middle-age and older adults diagnosed with essential hypertension to demographically matched normot

186 respond better than unselected patients with essential hypertension to endothelin receptor blockers.

187 most efficacious agents in the treatment of essential hypertension, understanding the pathogenesis o

188 nd composition in human subjects with PA and essential hypertension using contrast-enhanced cardiac m

189 Essential hypertension usually clusters with other cardi

190 edisposing to common disorders such as human essential hypertension we may gain insights into novel p

191 and the type I (AT1) angiotensin receptor in essential hypertension, we developed an experimental mod

192 Patients eligible for enrolment had essential hypertension, were aged 18 years or older, and

193 ould be used as monotherapy for treatment of essential hypertension, whereas low-dose HCTZ monotherap

194 Essential hypertension, which accounts for 90%-95% of al

195 could partially explain the pathogenesis of essential hypertension, which remains enigmatic in 95% o

196 component of therapy in young patients with essential hypertension who are overweight.

197 121 adults with essential hypertension who were under evaluation for a c

198 gal abnormalities that have been reported in essential hypertension, with emphasis on their role as p