ライフサイエンスコーパス: hypertensive

1 atistically significant differences in being hypertensive.

2 ducation, 28.1% were diabetic and 56.9% were hypertensive.

3 cantly advanced bone ages and are oftentimes hypertensive.

4 wed that Mcoln1(-/-) mice were spontaneously hypertensive.

5 renal abnormalities, and 35% of adults were hypertensive.

6 glaucoma suspects, and 108 eyes were ocular hypertensives.

7 were women, 25% were diabetic, and 91% were hypertensive; 104 started intervention, and 92 completed

8 s; 41% were black; 55% were female; 59% were hypertensive; 22% were diabetic; and 15% were current sm

9 MS with one or more VRF (80 ever-smokers, 43 hypertensives, 25 dyslipidaemics and 10 diabetics) were

10 , insulin (51.7% vs 38.3%, P = 0.0341), anti-hypertensive (41.1% vs 26.0%, P < 0.0001), and cholester

11 68%), obese (median body mass index 41), and hypertensive (98%), with clinical HF characterized by 65

12 A list of 35 peptides with potential hypertensive activity due to ACE inhibition were identif

13 KEY POINTS: In hypertensive adults (HTN), cardiovascular risk increases

14 f a multicenter randomized clinical trial of hypertensive adults 50 years or older without a history

15 Among hypertensive adults, declining kidney function measured

16 Among hypertensive adults, targeting an SBP of less than 120 m

17 nificantly associated with LE-PAD in Chinese hypertensive adults.

18 A slightly larger proportion of ocular hypertensive and glaucoma patients treated first with me

19 WNK1 and WNK4 in humans lead to a Mendelian hypertensive and hyperkalemic disease pseudohypoaldoster

20 tor, we found a good correlation between the hypertensive and LPA(4) agonistic activities.

21 alue of DSE was similar for patients who had hypertensive and normal BP responses (69% versus 73%; P=

22 rocedures were younger and less likely to be hypertensive and smokers.

23 s blood pressure in both individuals who are hypertensive and those who are normotensive, additively

24 a male recipient), lower ejection fraction, hypertensive, and had a history of smoking, alcohol, or

25 omen with T2DM were more likely to be obese, hypertensive, and have hypercholesterolemia, but were le

26 e despite recovery from motor deficits, with hypertensive animals showing some symptoms of anhedonia.

27 ty of hypothalamic presympathetic neurons in hypertensive animals.

28 pressure and sympathetic nerve discharges in hypertensive animals.

29 Background changes of hypertensive arterionephrosclerosis and diabetic glomeru

30 directly compared the relative importance of hypertensive arteriopathy and CAA scores as predictors o

31 d for global SVD burden, and SVD subtypes of hypertensive arteriopathy and cerebral amyloid angiopath

32 In dominance analysis, hypertensive arteriopathy score outperformed CAA in pred

33 s associated with SVD, particularly with the hypertensive arteriopathy subtype of SVD.

34 markers, particularly in regions typical of hypertensive arteriopathy: deep microbleeds (beta=0.63,

35 Women were older and more often obese and hypertensive but less likely to have coronary artery dis

36 Mice were made hypertensive by administration of angiotensin II via osm

37 One notable exception is black hypertensive candidates, who are frequently excluded reg

38 2005, programs have become more accepting of hypertensive candidates: 65% in 2017% vs 41% in 2005 con

39 To investigate the effect of SCFAs on hypertensive cardiac damage and atherosclerosis, wild-ty

40 been observed in several diseases, including hypertensive cardiac hypertrophy, Hirschsprung disease a

41 e lipotoxic and induce non-ischaemic and non-hypertensive cardiomyopathy, termed diabetic or lipotoxi

42 ly prevalent chronic disease associated with hypertensive cardiomyopathy.

43 (SHR) exhibiting many features of the human hypertensive cardiomyopathy.

44 FA propionate in 2 different mouse models of hypertensive cardiovascular damage.

45 ogical preventive strategy for patients with hypertensive cardiovascular disease.

46 n normal individuals versus those with early hypertensive changes according to the current ESC/ESH gu

47 in sheep with normotension (control) or with hypertensive chronic kidney disease (CKD).

48 In hypertensive CKD sheep, RDN reduced blood pressure and i

49 R2 protein were detected in renal samples of hypertensive compared with normotensive human subjects.

50 A total of 22 hypertensive control subjects and 98 HFpEF subjects unde

51 -HTN; n = 17), normotensive (NC; n = 17) and hypertensive controls (HTN; n = 16).

52 dings suggest that continued ACEi/ARB use in hypertensive COVID-19 patients yields better clinical ou

53 Irreversible MAOIs cause serious hypertensive crises owing to peripheral accumulation of

54 extreme blood pressure lability with severe hypertensive crises, hypotensive episodes, and orthostat

55 red were older and more likely obese, black, hypertensive, diabetic, hepatitis C positive, smokers, P

56 rtality ratio, 0.96; 95% CI, 0.74-1.22), for hypertensive direct causes (area under the curve, 0.81;

57 n reuptake inhibitor is also associated with hypertensive disease of pregnancy and cesarean delivery.

58 Preeclampsia (PE) is a hypertensive disease of pregnancy associated with substa

59 re during pregnancy (eg, maternal smoking or hypertensive disease) were not associated with higher su

60 ease groups (inflammatory polyarthropathies, hypertensive disease, circulatory disease, and metabolic

61 aorta and coronary artery atheroma, cardiac hypertensive disease, myocardial infarction and ischaemi

62 Preeclampsia is a pregnancy-related hypertensive disorder accounting for 14% of global mater

63 History of a hypertensive disorder of pregnancy (HDP) among women may

64 Pre-eclampsia is a severe hypertensive disorder of pregnancy and could lead to sev

65 5 (17.9%) women with eclampsia, stroke, or a hypertensive disorder of pregnancy causing intensive car

66 rder of pregnancy, and maternal death from a hypertensive disorder of pregnancy were prospectively co

67 Preeclampsia is a dangerous hypertensive disorder of pregnancy with known links to n

68 , stroke, admission to intensive care with a hypertensive disorder of pregnancy, and maternal death f

69 Preeclampsia is a hypertensive disorder of pregnancy.

70 nal death or intensive care admission with a hypertensive disorder of pregnancy.

71 Preeclampsia (PE) is a pregnancy specific hypertensive disorder.

72 nderlying causes of stillbirth were maternal hypertensive disorders (16.3%), placental separation and

73 14; 95% CI, 0.40-3.22) and pregnancy-induced hypertensive disorders (aOR, 1.24; 95% CI, 0.80-1.92).

74 es - with a higher prevalence when including hypertensive disorders - and is the leading cause of mat

75 The associations between pregnancy hypertensive disorders and common cardiovascular disorde

76 al lupus (OR(adj) 4.36, 95% CI [2.32-8.18]), hypertensive disorders in pregnancy (OR(adj) 2.72, 95% C

77 early pregnancy, extracted data on diabetes/hypertensive disorders in pregnancy from medical records

78 of women who delivered before 34 weeks with hypertensive disorders of pregnancy (0.38 [0.17-0.85], p

79 further 51 died from other complications of hypertensive disorders of pregnancy (0.95/10,000).

80 Hypertensive disorders of pregnancy (HDP) and gestationa

81 Hypertensive disorders of pregnancy (HDP) are a leading

82 Hypertensive disorders of pregnancy (HDP) are associated

83 whose first pregnancy was not complicated by hypertensive disorders of pregnancy (HR, 2.01; 95% CI, 1

84 rs: beta = 1.83 mm Hg (95% CI: 0.06, 3.60)), hypertensive disorders of pregnancy (vs.

85 Obstetric haemorrhage, sepsis, and hypertensive disorders of pregnancy account for more tha

86 of eclampsia and related complications from hypertensive disorders of pregnancy across 10 low- and m

87 Hypertensive disorders of pregnancy are associated with

88 psia and maternal and neonatal fatality from hypertensive disorders of pregnancy between countries em

89 Reducing deaths from hypertensive disorders of pregnancy is a global priority

90 spring congenital heart defects and maternal hypertensive disorders of pregnancy overall and for spec

91 Hypertensive disorders of pregnancy should be considered

92 proximately 42,000 women died as a result of hypertensive disorders of pregnancy worldwide; over 99%

93 ng SBP trajectories by gestational diabetes, hypertensive disorders of pregnancy, and formula milk in

94 women and in women with older maternal age, hypertensive disorders of pregnancy, and multiple gestat

95 models to determine the associations between hypertensive disorders of pregnancy, and preeclampsia al

96 tigate the association between preeclampsia, hypertensive disorders of pregnancy, and subsequent diag

97 not provide evidence for an association with hypertensive disorders of pregnancy, fetal growth, or ge

98 al population is also related to the risk of hypertensive disorders of pregnancy, including pre-eclam

99 Hypertensive disorders of pregnancy, including preeclamp

100 ional studies of the association between the hypertensive disorders of pregnancy, placental abruption

101 ar patterns of association were observed for hypertensive disorders of pregnancy, while preterm preec

102 Hypertensive disorders of pregnancy-chronic hypertension

103 nequity persist in healthcare for women with hypertensive disorders of pregnancy.

104 ring pregnancy, and has been associated with hypertensive disorders of pregnancy.

105 antagonists may provide a path for treating hypertensive disorders when small-molecule drugs targeti

106 Cardiac conditions during pregnancy include hypertensive disorders, hypercholesterolemia, myocardial

107 ers and children associated with gestational hypertensive disorders, in particular, preterm preeclamp

108 luding maternal overweight/obesity, diabetes/hypertensive disorders, or mood/anxiety disorders, incre

109 l growth and adiposity and pregnancy-related hypertensive disorders.

110 terone excess is a pathogenic factor in many hypertensive disorders.

111 , an L-type calcium channel blocker and anti-hypertensive drug, induces autophagy and clears diverse

112 An anti-hypertensive drug, reserpine, suppressed TEV uptake and

113 et cardiovascular risk factors (such as anti-hypertensive drugs, anti-platelet agents and statins) se

114 ypertensive injuries without influencing the hypertensive effect of angiotensin II.

115 pathy syndrome (PRES), also called the acute hypertensive encephalopathy and reversible posterior leu

116 ative wound and haematoma infection, grade 4 hypertensive encephalopathy, grade 3 acute cardiac failu

117 tory therapies have been shown to ameliorate hypertensive end-organ damage.

118 No other cause for the transient acute hypertensive episode were found.

119 ension, but can be added to control residual hypertensive episodes, often triggered by mental stress

120 was greater than 1.1, suggestive of a portal hypertensive etiology.

121 6 cohorts; n=4232 fistulas), and 0.03 venous hypertensive events (1 cohort; n=350 fistulas).

122 No patients had drug-related acute hypertensive events during or after the administration o

123 Blood pressure was similar among all hypertensive experimental groups.

124 fied a K572Q mutation in ADD3 in fawn-hooded hypertensive (FHH) rats-a mutation previously reported i

125 tion of specific peptides, particularly anti-hypertensives, from yogurt compared with their milk coun

126 y play a greater role in the pathogenesis of hypertensive glomerulosclerosis than previously thought.

127 No difference was found between the hypertensive group and healthy group in demographic and

128 biological outcomes when stratified based on hypertensive group.

129 ed in isolated myocardium from patients with hypertensive heart disease (HHD) and heart failure with

130 cognition and interoception in patients with hypertensive heart disease (HHD).

131 arrest, one gastric adenocarcinoma, and one hypertensive heart disease and congestive cardiac failur

132 nced higher mortality rates for ischemic and hypertensive heart disease compared with other subgroups

133 isease (371266 coronary heart disease, 35019 hypertensive heart disease, and 99815 other cardiovascul

134 he human heart and mouse models of ischemia, hypertensive heart disease, and aortic stenosis.

135 likely contributes to the modern epidemic of hypertensive heart disease.

136 sure overload are valuable for understanding hypertensive heart disease.

137 .5 vs 5.1 deaths per 100000 persons) to 4.2 (hypertensive heart disease: 4.3 vs 17.9 deaths per 10000

138 The diabetic, hypertensive heart failure rat (mRen27/tetO-shIR) were t

139 he mechanisms involved in protecting against hypertensive heart failure.

140 Male, Sprague-Dawley and Spontaneously-Hypertensive-Heart-Failure (SHHF) rats were treated oral

141 in a cross-sectional study including grade 1 hypertensive (HT) and normotensive (NT) subjects.

142 Renal proximal tubule (RPT) cells from hypertensive (HT) Euro-American males had deficient SNX1

143 FHL2 was abundantly upregulated in hypertensive human glomeruli and animal kidney samples.

144 e mutations have been found predominantly in hypertensive human subjects.

145 in the smooth muscle layer of arteries from hypertensive humans and that Tyr(198) phosphorylation is

146 mbrane-associated PANX1 in small arteries of hypertensive humans.

147 We found that the SHRSP rats were hypertensive, hyperphagic, less sensitive to hypophagic

148 er, the current meta-analysis suggested that hypertensive individuals may also be at higher risk of c

149 ized controlled trials allocating healthy or hypertensive individuals to SR or usual sodium intake.

150 s in the elaboration of functional foods for hypertensive individuals.

151 of 1.58 (1.04-2.41) among prehypertensive or hypertensive individuals.

152 thologies of inflammatory, hypoxic, ischemic/hypertensive, infectious and thrombotic etiologies were

153 s a global protective role during glomerular hypertensive injuries without influencing the hypertensi

154 ons and protects glomerular capillaries from hypertensive injury.

155 proteomic strategy to analyze the effect of hypertensive insults on kidneys.

156 pressure may contribute to poor outcomes in hypertensive intraventricular hemorrhage.

157 , multilayered omics provides an overview of hypertensive kidney damage and suggests that metabolic o

158 litate a potential noninvasive detection for hypertensive kidney injury.

159 oRNA (miRNA) as a non-invasive biomarker for hypertensive kidney injury.

160 blockers (ARB) during hospitalization of 614 hypertensive laboratory-confirmed COVID-19 patients.

161 Among people with hypertensive levels of blood pressure, use of any AHM wi

162 fusion following a 2-week withdrawal of anti-hypertensive medications.

163 in control and AngII infused (490 ng/kg/min) hypertensive mice.

164 administration and treatment compared to the hypertensive models.

165 Mb significantly decreased blood pressure in hypertensive models.

166 f C1 neurons during specific behaviors or in hypertensive models.

167 ery (PCA) occlusion in old, atherosclerotic, hypertensive monkeys to that in young monkeys.

168 Ascites syndrome is a hypertensive, multifactorial, multigene trait affecting

169 Here we show that hypertensive nephropathy (HN) patients and AngII-infused

170 el to determine the possible role of FHL2 in hypertensive nephropathy.

171 have a pathogenic role in the development of hypertensive nephropathy.

172 into a 44-year-old female with a history of hypertensive nephrosclerosis and anuria on dialysis for

173 ts (GON and normal visual field), and ocular hypertensives (normal disc, normal visual field, and int

174 Chronically hypertensive (one-kidney-one-clip surgery) wild-type and

175 ssment, and clinical ascertainment of ocular hypertensive or glaucoma status (including glaucoma susp

176 85 to 0.95]) and cardiovascular mortality in hypertensive participants (RR, 0.67 [CI, 0.46 to 0.99]).

177 Subgroup analyses showed that hypertensive participants had stronger inverse associati

178 ential strain in participants with diabetes, hypertensive participants, and participants with a previ

179 and sex-matched RA-normotensive (n = 13), RA-hypertensive patients (RA-HTN; n = 17), normotensive (NC

180 y of the RI was examined in 256 asymptomatic hypertensive patients and 10 patients with heart failure

181 nce of this ADAM17-mediated ACE2 shedding in hypertensive patients and further identify the cell type

182 PAMM lesions were found in 24 of 27 (88.9%) hypertensive patients and in 4 of 24 (16.7%) healthy ind

183 ss, reflecting subclinical oedema, occurs in hypertensive patients and in association with aging.

184 that RI provides an approach for stratifying hypertensive patients and is suitable for testing in oth

185 Chronic PAMM lesions are highly prevalent in hypertensive patients and may represent the earliest cha

186 l metabolites in the systemic circulation of hypertensive patients and rodent models of hypertension.

187 an matched case-control studies, 1 nested in hypertensive patients and the other in patients with car

188 studies in both drug-naive and drug-treated hypertensive patients demonstrated a significant reducti

189 hypertension therapy, significant numbers of hypertensive patients fail to achieve recommended blood

190 in normotensive Afro-Caribbean people and in hypertensive patients of all ethnic origins.

191 lony-forming cells from idiopathic pulmonary hypertensive patients showed upregulation of CLIC4 expre

192 between the ADC value and systolic strain in hypertensive patients with left ventricular hypertrophy

193 Greece, Ireland, Japan, the UK, and the USA, hypertensive patients with office systolic blood pressur

194 h left ventricular hypertrophy (HTN LVH) and hypertensive patients without LVH (HTN non-LVH) using ca

195 alanced data set of 24,434 with (69.71%) non-hypertensive patients, and (30.29%) hypertensive patient

196 particularly beneficial in some subgroups of hypertensive patients, as those who are at highest cardi

197 Among hypertensive patients, awareness, treatment, and control

198 In hypertensive patients, endothelial microparticles indeed

199 Two hundred fifty-six overweight or obese hypertensive patients, including 54% black and Hispanic

200 In older hypertensive patients, intensive BP control (systolic BP

201 DAM17-mediated ACE2 shedding in the brain of hypertensive patients, leading to a loss in compensatory

202 de (HCTZ) in reducing blood pressure (BP) in hypertensive patients, though both are plagued with BP r

203 and support in the control and detection of hypertensive patients, which is part of the critical fac

204 ACE2 activity in the cerebrospinal fluid of hypertensive patients, which was correlated with systoli

205 at may be triggered simultaneously in septic hypertensive patients.

206 ssociated with ventricular hypertrophy in AA hypertensive patients.

207 71%) non-hypertensive patients, and (30.29%) hypertensive patients.

208 pe 2 diabetes, reduce blood pressure (BP) in hypertensive patients.

209 ary care providers and their black and white hypertensive patients.

210 e intervals in 155 healthy volunteers and 40 hypertensive patients.

211 age, smoking, kidney disease and diabetes in hypertensive patients.

212 olites are similar in healthy volunteers and hypertensive patients.

213 Incidence of the hypertensive phase (defined as intraocular pressure [IOP

214 ) and 55.0% (11/20) of the cases exhibited a hypertensive phase (P = 0.04), respectively.

215 tion) in the prevention of the postoperative hypertensive phase and on long-term intraocular pressure

216 tion of AGV experienced a lower incidence of hypertensive phase and required fewer medications when u

217 ermediate postoperative period and blunt the hypertensive phase compared with AGV implantation alone.

218 The frequency of hypertensive phase was 61.5% in control eyes and 38.5% i

219 Frequency of hypertensive phase was also determined.

220 Mice lacking RGS2 display a hypertensive phenotype, and several RGS2 missense mutati

221 ic mice recapitulated the prebiotic-deprived hypertensive phenotype, including cardiac manifestations

222 annels (KCNT1 and KCNT2) shows only a modest hypertensive phenotype.

223 trictive agents, thus producing a paroxysmal-hypertensive phenotype.

224 extracellular matrix (ECM) may induce ocular hypertensive phenotypes in human TM (hTM) cells to cause

225 ht into which patients in this heterogeneous hypertensive population are most likely to respond favor

226 n-III, in BP lowering in a high-risk diverse hypertensive population.

227 checks of those peptides based on their anti-hypertensive potentialities.

228 undation for exploring similar mechanisms in hypertensive pregnancies.

229 s drive detrimental TGFbeta1 pathways in the hypertensive pulmonary vasculature.

230 ely ablate the CB in vivo in a spontaneously hypertensive rat (SHR) model of hypertension.

231 is study, we hypothesized that spontaneously hypertensive rat (SHR) vessels should have a smaller num

232 microstructure of healthy and spontaneously hypertensive rat hearts at the ages of 12 and 24 months.

233 At advanced stages of FSGS, fawn-hooded hypertensive rat kidneys exhibited distinctly increased

234 ducible diabetes was crossed with the mRen27 hypertensive rat to create a novel model for heart failu

235 promotes eNOS uncoupling in normotensive and hypertensive rat vessels and in HUVECs.

236 Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto ra

237 We used Spontaneously Hypertensive Rats (SHR) exhibiting many features of the

238 Spontaneously hypertensive rats (SHR) were compared to normotensive ra

239 Spontaneously hypertensive rats (SHR) were treated with the NK-1R anta

240 SI; at a septic-like model) in spontaneously hypertensive rats (SHR).

241 development of hypertension in spontaneously hypertensive rats (SHR).

242 to suppress blood pressure in spontaneously hypertensive rats (SHR).

243 f amaranth protein/peptides on spontaneously hypertensive rats (SHR).

244 rve effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explore its possible mechan

245 Two cohorts of Spontaneously Hypertensive Rats (SHRs) were exposed to 150 or 500 mug/

246 between Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHRs), renal ETBR phosphorylation was

247 ally projecting PVN neurons in spontaneously hypertensive rats (SHRs).

248 emale 16 week old stroke prone spontaneously hypertensive rats (SHRSP).

249 beta1 link was also evident in spontaneously hypertensive rats and DDR2-knockout mice.

250 e sufficient to reduce the blood pressure in hypertensive rats and justify further investigation in l

251 was also investigated in SHR (spontaneously hypertensive rats).

252 sulin resistance and BP in the spontaneously hypertensive rats.

253 e and increased firing activity of MNCs from hypertensive rats.

254 s STIM1, which is up-regulated in VSMCs from hypertensive rats.

255 from these regions have been associated with hypertensive-related traits in human association studies

256 CI: 0.90, 1.19) if they were normotensive or hypertensive, respectively (P-interaction = 0.003).

257 Patients with hypertensive response (n=1905; 9%) were more likely to h

258 h WT (wild type) controls had an exaggerated hypertensive response and augmented proportions of CD62L

259 =70% stenosis) was lower in patients who had hypertensive response compared with those who had normal

260 Patients with hypertensive response during DSE are more likely to have

261 EM) cells in the bone marrow and reduced the hypertensive response to a subsequent response to low do

262 females have lower BP before age 60, blunted hypertensive response to angiotensin II, and a leftward

263 n transferred to recipients lacking IgG; the hypertensive response was absent if recipients were Fcga

264 The LPA-induced hypertensive response was significantly attenuated by pr

265 ble effects on renal sodium handling and the hypertensive response, accruing from the functions of th

266 cohort was responsible for their exaggerated hypertensive response, we chronically infused Ang II int

267 PA(6), also showed an attenuated LPA-induced hypertensive response.

268 lecular mechanism underlying the LPA-induced hypertensive response.

269 which contained abundant LPA, also induced a hypertensive response.

270 Micu2 in regulating angiotensin II-mediated hypertensive responses that are critical in protecting t

271 r vision (41.9%), screening for diabetic and hypertensive retinopathy (13.1%), referral (9.7%), sudde

272 Hypertensive retinopathy (18.9%) was the commonest VR di

273 al-time PCR in MNCs in sham and renovascular hypertensive (RVH) rats.

274 neurosecretory cells (MNCs) in renovascular hypertensive (RVH) rats.

275 muscle cells of renal resistance vessels of hypertensive salt-sensitive rats and is involved in the

276 for discrimination between normotensive and hypertensive samples.

277 ne users), and 6.4% of control subjects were hypertensive (SBP >/=140 and/or DBP >/=90 mm Hg) versus

278 Wistar-Kyoto (WKY) rat and the spontaneously hypertensive (SH) rat to inhalation and intravenous inje

279 ve Wistar-Kyoto (WKY) rats and spontaneously hypertensive (SH) rats.

280 netics in male young and adult spontaneously hypertensive (SHR) rats compared with age-matched normot

281 ce to hypertension in the presence of a mild hypertensive stimulus, with resultant pathological cardi

282 and can be reactivated on reexposure to the hypertensive stimulus.

283 ere we report that concomitant metabolic and hypertensive stress in mice-elicited by a combination of

284 ctors of metabolic syndrome in spontaneously hypertensive stroke-prone (SHRSP) and Wistar-Kyoto (WKY)

285 ition to metabolic syndrome in spontaneously hypertensive stroke-prone rats.

286 ls) activity, VCAM, ICAM, and MCP1 levels in hypertensive subjects compared with normotensive subject

287 effects of lowering blood pressure in older hypertensive subjects even after the age of 80 years.

288 at the lowest doses that prevent the largest hypertensive surges.

289 AC) can further guide the allocation of anti-hypertensive treatment intensity.

290 Tyr(198)-phosphorylated PANX1 is involved in hypertensive vascular pathology.

291 rotein and activity were up-regulated in the hypertensive vasculature.

292 [50% female; 52 (17) (mean (SD)) years; 25% hypertensive] were studied.

293 nts -217A, -6A, +507G, and +1164A and is pro-hypertensive, whereas Hap-II contains the variants -217G

294 n of PKG1alpha and lowered blood pressure in hypertensive wild-type mice, but not C42S PKG1alpha knoc

295 and heart failure in sedentary, chronically hypertensive wild-type mice.

296 comatous eyes, glaucoma suspects, and ocular hypertensives with 24-2 and 10-2 visual fields.

297 tion of CCB or ACEi use and breast cancer in hypertensive women aged >/=55 years at 3 sites in the Ka

298 diuretics (TD) are commonly prescribed anti-hypertensives worldwide.

299 on in ZSF1 obese rats and to compare it with hypertensive ZSF1 lean and healthy Wistar-Kyoto controls

300 to phenylephrine were similarly increased in hypertensive ZSF1 lean and obese, only ZSF1 obese showed