ライフサイエンスコーパス: renal vasoconstriction

1 eptors contribute importantly to this reflex renal vasoconstriction.

2 emia, which may contribute to the associated renal vasoconstriction.

3 mbined with other agents that may potentiate renal vasoconstriction.

4 of control subjects, despite greater resting renal vasoconstriction.

5 ng renal sodium retention, renin release and renal vasoconstriction.

6 pathogenesis is rooted in marked maladaptive renal vasoconstriction.

7 ificant mesenteric and hindquarters, but not renal, vasoconstrictions.

8 In conclusion, AngII can elicit renal vasoconstriction, albeit attenuated, in AT1A knock

9 h before intravenous LPS abolished the early renal vasoconstriction and alleviated the decrease in GF

10 nist (SQ29,548), would alleviate LPS-induced renal vasoconstriction and ARF.

11 tes the muscle metaboreflex producing reflex renal vasoconstriction and decreased renal blood flow, w

12 In addition, ERAs can ameliorate CNI-induced renal vasoconstriction and improve proteinuria and prese

13 ia is a form of fetal stress that stimulates renal vasoconstriction and ischaemia as a consequence of

14 sporine (CsA) or tacrolimus (FK506) leads to renal vasoconstriction and nephrotoxicity.

15 intrarenal hemodynamics demonstrated severe renal vasoconstriction and preferential cortical ischemi

16 hypothesized that serelaxin could ameliorate renal vasoconstriction and renal dysfunction in patients

17 deposition of myoglobin in the kidney causes renal vasoconstriction and renal failure.

18 e renal failure, frequently a consequence of renal vasoconstriction and subsequent renal ischemia, is

19 between hypertension and kidney disease via renal vasoconstriction and systemic hypertension.

20 genic response by NO, norepinephrine-induced renal vasoconstriction, and acetylcholine- or NO-induced

21 methyl ester (L-NAME) leads to hypertension, renal vasoconstriction, and natriuresis in rats with int

22 imal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure.

23 imal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure.

24 e, both the magnitude and duration of reflex renal vasoconstriction are exaggerated in heart failure

25 2-CA evoked bradycardia and renal vasoconstriction, as in 3-day-old piglets, but als

26 A; 30 mg kg(-1) i.v.) evoked bradycardia and renal vasoconstriction, but had no effect on femoral vas

27 contribution to the ventilatory response, or renal vasoconstriction, but is largely responsible for h

28 ycardia and a rise in arterial pressure with renal vasoconstriction, but no change in renal blood flo

29 Extreme renal vasoconstriction characterizes hepatorenal syndrom

30 a pig model to determine whether CsA-induced renal vasoconstriction could be detected, thus offering

31 tially responsible for the cisplatin-induced renal vasoconstriction demonstrable in the in vivo model

32 esent study examined the hypothesis that the renal vasoconstriction during endotoxemia occurs in part

33 These results demonstrate that renal vasoconstriction during endotoxemic shock induced

34 t is unknown whether there is further reflex renal vasoconstriction during exercise.

35 Muscle mechanoreflex mediated renal vasoconstriction during short bouts of HG is not i

36 n ventilation evoked by 10 and 6% O2 and the renal vasoconstriction evoked by 10% O2, but had no effe

37 AngII produced greater renal vasoconstriction in 7-wk-old, spontaneously hypert

38 ANG II produced less pronounced renal vasoconstriction in rats fed a low- compared with

39 selective, AT1 receptor blocker, inhibiting renal vasoconstriction in rodents in a concentration- an

40 nograms of AngII were required to elicit 20% renal vasoconstriction in these mutant mice.

41 etting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, p

42 on of small kidneys than large ones, and the renal vasoconstriction induced by SWL was greatest in sm

43 injury using an experimental model in which renal vasoconstriction is believed to cause ischemic ren

44 tion of the muscle metaboreceptors to reflex renal vasoconstriction is blunted in heart failure patie

45 orm of renal dysfunction for which excessive renal vasoconstriction is one of the main, but not the o

46 While it is well documented that renal vasoconstriction leading to impaired renal functio

47 Renal vasoconstriction markedly contrasts with sepsis-in

48 tor to the secondary fall in ventilation and renal vasoconstriction respectively, whereas at 3 weeks,

49 nal syndrome result from water retention and renal vasoconstriction, respectively, both of which are

50 ation and in larger doses preferential extra-renal vasoconstriction resulting in redistribution of bl

51 Renal vasoconstriction returned to baseline in normal hu

52 ved severely (SD) diabetic rats that display renal vasoconstriction show reduced levels and excretion

53 on, and ET-1 plays a key role in CNI-induced renal vasoconstriction, sodium retention, and hypertensi

54 ndogenous ET contributes to the systemic and renal vasoconstriction that characterizes this model of

55 ptors in patients with CHF results in marked renal vasoconstriction that leads to an important reduct

56 In fact, the increase in renal vasoconstriction was blunted in heart failure pati

57 with intravenous candesartan, AngII-induced renal vasoconstriction was inhibited dose dependently up

58 which isolates muscle metaboreceptors, peak renal vasoconstriction was not greater in heart failure

59 have been expected if angiotensin-dependent renal vasoconstriction was responsible for the renal vas

60 ip (30% maximum voluntary contraction), peak renal vasoconstriction was significantly increased in he

61 Acute endotoxemic renal failure involves renal vasoconstriction, which presumably occurs despite

62 Therapeutic targeting of renal vasoconstriction with serelaxin in the rat models

63 in ventilation, a gradual tachycardia and a renal vasoconstriction, with an increase in femoral bloo