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 ificant mesenteric and hindquarters, but not renal, vasoconstrictions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

22 2-CA evoked bradycardia and renal vasoconstriction, as in 3-day-old piglets, but als

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

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

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

26 Extreme renal vasoconstriction characterizes hepatorenal syndrom

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

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

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

30 These results demonstrate that renal vasoconstriction during endotoxemic shock induced

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

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

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

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

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

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

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

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

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

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

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

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

43 Renal vasoconstriction markedly contrasts with sepsis-in

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

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

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

47 Renal vasoconstriction returned to baseline in normal hu

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

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

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

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

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

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

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

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

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

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

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

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