ライフサイエンスコーパス: severe hypertension

1 ormone aldosterone and are a common cause of severe hypertension.

2 nd further raises blood pressure, leading to severe hypertension.

3 n of kidney dysfunction and outcome in acute severe hypertension.

4 outcome in patients hospitalized with acute severe hypertension.

5 ension are rare genetic disorders that cause severe hypertension.

6 Cyp4a14, a murine homologue of CYP4A11, have severe hypertension.

7 e rats (SHR), a widely used genetic model of severe hypertension.

8 mented sympathetic output compared with more severe hypertension.

9 reated groups progressed from less severe to severe hypertension.

10 ian guideline adherence in the management of severe hypertension.

11 cardial reperfusion injury in the setting of severe hypertension.

12 However, 1K1C produced more severe hypertension (164+/-2 mm Hg) and cardiac hypertro

13 Few women were eligible for methyldopa for severe hypertension (181 [1%] of 20 819) or intramuscula

14 f 1115 [9%]), hypotension (89 of 1115 [8%]), severe hypertension (61 of 1115 [5%]), and coronary mech

15 t accepted treatment (162 [89.5%] of 181 for severe hypertension and 133 [67.2%] of 198 for pre-eclam

16 mably as a consequence of abrupt, transient, severe hypertension and catecholamine release.

17 a showing that rare mutations in PPARy cause severe hypertension and clinical trial data which show t

18 adults >=40 years, identifying 266 (9%) with severe hypertension and enrolling 200 (98 telehealth arm

19 ing them significantly increases the risk of severe hypertension and heart failure.

20 in pathogenesis in a subset of patients with severe hypertension and implicate loss of K(+) channel s

21 ns transplanted per donor, but more cases of severe hypertension and tachycardia occurred in the levo

22 morbidity among patients admitted with acute severe hypertension, and AKI is a frequent form of acute

23 -protein signaling-2)-deficient mice exhibit severe hypertension, and genetic variations of RGS2 occu

24 gulator of G-protein signaling-2 (RGS2) have severe hypertension, and RGS2 genetic variations occur i

25 At baseline, patients had severe hypertension (aortic systolic pressure, 176+/-26

26 ms and provided DNA samples but did not have severe hypertension, aortic prosthesis, or significant a

27 Mutations in Cul3 cause severe hypertension by affecting both renal and vascular

28 ovariate data, from 2,044 sibling pairs with severe hypertension, collected by the British Genetics o

29 nt improved hypertension control and reduced severe hypertension compared to clinic-based care.

30 nned delivery reduces maternal morbidity and severe hypertension compared with expectant management,

31 (STAT) registry enrolled patients with acute severe hypertension, defined as > or =1 blood pressure m

32 er, reported significantly more frequent and severe hypertension, diabetes, cancer, heart disease, ar

33 Dahl salt-sensitive rats develop severe hypertension during a high-sodium diet, but the b

34 on factor is required for the development of severe hypertension during chronic angiotensin II signal

35 outcomes; however, individuals with moderate-severe hypertension face additional barriers to care, in

36 roducing adrenal adenomas (APAs), a cause of severe hypertension, feature constitutive hormone produc

37 Severe hypertension (>/=160/110 mm Hg) developed in 40.6

38 A few forms of severe hypertension have been linked to single genes.

39 Severe hypertension in ACE2-deficient mice was associate

40 Renovascular disease is a frequent cause of severe hypertension in children and may result in signif

41 alol-are viable initial options for treating severe hypertension in low-resource settings.

42 retard, and methyldopa for the management of severe hypertension in pregnancy.

43 prove hypertension control among adults with severe hypertension in rural Uganda and Kenya.

44 e despite having no effect on the sustained, severe hypertension induced by L-NAME.

45 ehealth focused on individuals with moderate-severe hypertension is a promising approach to improve o

46 s were "poor maternal outcome" (composite of severe hypertension, maternal death, or maternal morbidi

47 entricular rhythm disorders (n = 22 [0.7%]), severe hypertension (n = 24 [0.8%]) and hypotension or l

48 with hypokalaemia, together with those with severe hypertension or a family history of hypertension

49 in undetermined, the current study rules out severe hypertension or advanced renal disease as sole ca

50 ng disease of pregnant women associated with severe hypertension, proteinuria, or multi-organ injurie

51 beta1 subunit during genetic borderline and severe hypertension reduced BK channel activity by decre

52 In an ASA subject with severe hypertension refractory to antihypertensive medic

53 Hg (normal, elevated, stage 1, stage 2, and severe hypertension, respectively).

54 d pharmacological blood pressure control for severe hypertension (systolic blood pressure >=160 mm Hg

55 However, so far, only patients with severe hypertension (systolic BP >/=160 mm Hg or >/=150

56 roup) or to receive no such treatment unless severe hypertension (systolic pressure, >=160 mm Hg; or

57 activated ion channel, in turn resulting in severe hypertension that is resistant to most forms of c

58 o not have acute organ injury in addition to severe hypertension, they benefit from a conservative, o

59 Regimens for the acute treatment of severe hypertension typically include intravenous medica

60 xonomy of suboptimal adherence scenarios for severe hypertension was developed and barriers to guidel

61 25 d after the induction of severe hypertension with deoxycorticosterone acetate and

62 KCNJ5 mutation in a Mendelian form of early severe hypertension with massive adrenal hyperplasia.

63 duced FBF, altered flow distribution, and/or severe hypertension with the progression toward diabetes

64 n a strategy of reserving treatment only for severe hypertension, with no increase in the risk of sma

65 e aldosterone and cause millions of cases of severe hypertension worldwide.