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1 s whether under normokalaemic (5.2 mM K+) or hypokalaemic (3.0 mM K+) conditions, in both the presenc
2          Analysis of patients with inherited hypokalaemic alkalosis resulting from salt-wasting has p
3                                    Inherited hypokalaemic alkalosis with low blood pressure can be di
4 arbour CLCNKB mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pres
5 ar classification of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes
6  Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pre
7                                 Patients are hypokalaemic and hypomagnesaemic, with reduced interstit
8                                        Under hypokalaemic conditions, both human cardiomyocytes deriv
9 gs empirically associate arrhythmogenesis in hypokalaemic hearts with transient alterations in transm
10 alities in electrolyte homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome re
11 nitiated arrhythmic activity specifically in hypokalaemic (n = 8, five hearts) as opposed to normokal
12 reated normokalaemic (n = 8, five hearts) or hypokalaemic (n = 8, five hearts) hearts.
13 ic (n = 25, 14 hearts), or lidocaine-treated hypokalaemic (n = 8, five hearts) or normokalaemic heart
14 laemic (5.5 +/- 4.5 ms, n = 8, five hearts), hypokalaemic (n = 8, five hearts), or lidocaine-treated
15 , could contribute towards the appearance of hypokalaemic paralysis in the affected individual.
16 basis for depolarization-induced weakness in hypokalaemic periodic paralysis (HypoPP) arising from mu
17                                              Hypokalaemic periodic paralysis (hypoPP) is the archetyp
18 ates that 90% of the known mutations causing hypokalaemic periodic paralysis (HypoPP) result in loss
19 ss of force induced by a low-K+ challenge in hypokalaemic periodic paralysis (HypoPP).
20 ) reabsorption in proximal tubule cells) and hypokalaemic periodic paralysis (hypoPP; usually associa
21             Three missense mutations causing hypokalaemic periodic paralysis (R528H in domain II S4 o
22 ive in preventing attacks in mouse models of hypokalaemic periodic paralysis and now needs to be test
23 loped a CaV1.1-R528H knock-in mouse model of hypokalaemic periodic paralysis and show herein that bum
24             Transient attacks of weakness in hypokalaemic periodic paralysis are caused by reduced fi
25 lishes bumetanide as a potential therapy for hypokalaemic periodic paralysis arising from either NaV1
26 etazolamide has been used as a treatment for hypokalaemic periodic paralysis for over 40 years but it
27                          In a mouse model of hypokalaemic periodic paralysis from a sodium channel mu
28 rginine residues in an S4 segment that cause hypokalaemic periodic paralysis induce a hyperpolarizati
29 other recent study indicated that thyrotoxic hypokalaemic periodic paralysis is determined by mutatio
30                                              Hypokalaemic periodic paralysis is typically associated
31  mechanism of disrupted S4 translocation for hypokalaemic periodic paralysis mutations at arginine re
32 cated that bumetanide can prevent attacks of hypokalaemic periodic paralysis, but this has not yet be
33 unction changes has an uncertain relation to hypokalaemic periodic paralysis.
34 mutations that cause gating pore current and hypokalaemic periodic paralysis.
35 and cytopathology that are characteristic of hypokalaemic periodic paralysis.
36 ave been established as a pathomechanism for hypokalaemic periodic paralysis.
37 encoding CaV1.1) is the most common cause of hypokalaemic periodic paralysis.
38        Potassium-depleted rats were markedly hypokalaemic (plasma potassium, 1.4 +/- 0.1 vs. 4.1 +/-