scholarly journals 1072-218 High prevalence in pharmacological responses mimic Brugada syndrome in Japanese—A pure Na channel blocker, pilsicainide challenge test in the normal heart

2004 ◽  
Vol 43 (5) ◽  
pp. A121
Author(s):  
Takeshi Ueyama ◽  
Akihiko Shimizu ◽  
Masahiro Esato ◽  
Ryousuke Kametani ◽  
Masashi Kanemoto ◽  
...  
Keyword(s):  
Brugada Syndrome ◽  
Channel Blocker ◽  
Challenge Test ◽  
Na Channel ◽  
Normal Heart ◽  
High Prevalence

Contractile responses to ouabain and K+-free solution in aorta from hypertensive rats

1986 ◽  
Vol 250 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
R. S. Moreland ◽  
T. C. Major ◽  
R. C. Webb
Keyword(s):  
Channel Blocker ◽  
Isometric Force ◽  
Maximal Response ◽  
Na Channel ◽  
Free Solution ◽  
Contractile Responses ◽  
Spontaneously Hypertensive ◽  
Force Development ◽  
Monensin A ◽  
Wistar Kyoto

This study characterizes isometric force development in response to ouabain and K+-free solution in isolated aortic strips from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. SHR aortas were more sensitive to ouabain than those from WKY (threshold: SHR, 3.1 X 10(-5) M; WKY, 25.6 X 10(-5) M), and force development in response to 10(-3) M ouabain was greater in SHR (SHR, 586 +/- 51 mg; WKY, 245 +/- 24 mg). Monensin, a Na+ ionophore, potentiated contractile responses to ouabain, whereas amiloride, a Na+ channel blocker, and low Na+ solutions depressed contractile responses to ouabain. Contractile responses of SHR aortic strips to K+-free solution were faster than those of WKY aortic strips [time to half-maximal response (t1/2): SHR, 24 +/- 5 min; WKY, 47 +/- 4 min]. Maximal force development by aortic strips from SHR in response to K+-free solution was not different from that of WKY aortic strips (SHR, 808 +/- 34 mg; WKY, 750 +/- 37 mg). Monensin (10(-5) M) increased the rate of force development to K+-free solution to a greater extent in WKY aortic strips than in those from SHR (t1/2: SHR, 3 +/- 1 min; WKY, 4 +/- 2 min). Amiloride and low Na+ solution depressed contractile responses to K+-free solution in both SHR and WKY aortic strips. These observations demonstrate that SHR aortas are more responsive to ouabain and K+-free solution compared with WKY aortas. Contractile responses to ouabain and K+-free solution were sensitive to experimental interventions that alter transmembrane Na+ movements.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals B-PO04-024 PREDICTION OF A POSITIVE SODIUM CHANNEL BLOCKER PROVOCATION TEST IN PATIENTS SUSPECTED OF BRUGADA SYNDROME

Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S289
Author(s):  
Martijn Hendrik van der Ree ◽  
Jeroen Vendrik ◽  
Tom E. Verstraelen ◽  
Jan A. Kors ◽  
Ahmad S. Amin ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Brugada Syndrome ◽  
Channel Blocker ◽  
Provocation Test ◽  
Sodium Channel Blocker

Abstract 5676: Elevated Oxidative Stress is Associated with Ventricular Fibrillation Episode in Patients with Brugada Syndrome without SCN5A Mutation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masamichi Tanaka ◽  
Keiko Ohgou ◽  
Koji Nakagawa ◽  
Takeshi Tada ◽  
Masato Murakami ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Ventricular Fibrillation ◽  
Brugada Syndrome ◽  
Endomyocardial Biopsy ◽  
Heart Diseases ◽  
Multivariable Analysis ◽  
Pathophysiological Mechanism ◽  
Normal Heart ◽  
Scn5a Mutation

Background; Brugada Syndrome (BS) is a disease known to cause ventricular fibrillation (VF) with structurally normal heart. Gene mutation (i.e. SCN5A) has been proposed to be related to the development of BS and VF. However, the pathophysiological mechanism associated with VF development without SCN5A mutation has not been studied yet. Oxidative stress is a common disorder that is related to many heart diseases. We have previously demonstrated that oxidative stress is closely linked to the arrhythmic development. Accordingly, we examined 4-hydroxy-2-nonenal (HNE) modified protein, which is a common mediator of oxidative stress in the myocardium, and VF episodes in patients with BS. Methods; We collected sixty-eight BS patients that underwent right ventricular endomyocardial biopsy (66 males, 2 female; mean age 49.0±11.6 years old). VF was documented in 11 and SCN5A mutation was detected in 14 patients. Biopsy samples were processed for histology [Masson’s trichrome staining for fibrosis, immuno staining for CD45, CD68, and HNE modified protein]. All results from histology were compared with VF episodes. We also performed the analysis in VF patients with (n=14) or without SCN5A mutations (n=54). Results: HNE positive area was significantly larger in VF patients [VF(+): 16.3±10.5, VF(−): 9.3±5.7%: P=0.029]. All other parameters (fibrosis area, CD45, and CD68) were not different between the groups. In multivariable analysis, HNE positive area was most important risk factor of VF development in patients without SCN5A mutation (P=0.004). Conclusions ; These data suggested that oxidative stress is associated with VF development in BS patients, especially in patients without SCN5A mutation.

Inhibition by extracellular Na+ replacement of GRF-induced GH secretion from rat pituitary cells

1988 ◽  
Vol 254 (4) ◽  
pp. E476-E481 ◽  
Author(s):  
M. Kato ◽  
M. A. Hattori ◽  
M. Suzuki
Keyword(s):  
Anterior Pituitary ◽  
Channel Blocker ◽  
Na Channel ◽  
Pituitary Cells ◽  
Ionic Mechanism ◽  
Camp Production ◽  
Normal Medium ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

To further clarify the ionic mechanism of the action of growth hormone (GH)-releasing factor (hGRF) on GH secretion, the involvement of extracellular Na+ was studied in perifused dispersed rat anterior pituitary cells. Replacing extracellular Na+ with mannitol or tris(hydroxymethyl)aminomethane (Tris+) suppressed hGRF- and dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced GH secretion. The peak responses to a 2-min application of 1 nM hGRF were 165.0 +/- 5.6 ng/ml (normal medium, mean +/- SE), 21.2 +/- 1.4 ng/ml (Na+-free, mannitol medium), and 18.0 +/- 1.7 ng/ml (Na+-free, Tris+ medium). GH secretion induced by DBcAMP was also suppressed by Na+ replacement to less than 50% of that in normal medium. However, either 15 or 30 mM KCl-stimulated GH secretion was not markedly affected by replacement of Na+ with either compound. Tetrodotoxin, a voltage-sensitive Na+ channel blocker, had no effect on either hGRF- or excess K+-induced GH secretion. cAMP production by hGRF was not greatly affected by replacing extracellular Na+. Thus extracellular Na+ plays an important role in hGRF-induced GH secretion, especially in the process after cAMP production. The involvement of cAMP-sensitive Na+ channels in hGRF-stimulated GH secretion is discussed.

scholarly journals Molecular basis of Na channel dysfunction of Brugada syndrome

1999 ◽  
Vol 79 ◽  
pp. 39
Author(s):  
Naomasa Makita ◽  
Nobumasa Shirai ◽  
Morio Kanno ◽  
Akira Kitabatake
Keyword(s):  
Brugada Syndrome ◽  
Molecular Basis ◽  
Na Channel

Mechanism of acidification along cortical distal tubule of the rat

1994 ◽  
Vol 266 (2) ◽  
pp. F218-F226 ◽  
Author(s):  
R. Fernandez ◽  
M. J. Lopes ◽  
R. F. de Lira ◽  
W. F. Dantas ◽  
E. J. Cragoe Junior ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Exchange Resin ◽  
Rat Kidney ◽  
Specific Inhibitor ◽  
Distal Tubule ◽  
Ringer Solution ◽  
Na Channel ◽  
Bafilomycin A1 ◽  
Bicarbonate Reabsorption ◽  
Distal Tubules

The cellular mechanism of luminal acidification (bicarbonate reabsorption) was studied in cortical distal tubules of rat kidney. The stopped-flow microperfusion technique was applied to early distal (ED) and late distal (LD) segments, perfused with bicarbonate Ringer solution to which specific inhibitors were added, to measure bicarbonate reabsorption [HCO3 flux (JHCO3)]. pH and transepithelial potential difference (Vt) were recorded by double-barreled H+ exchange resin/reference (1 M KCl) electrodes. Amiloride increased stationary pH and reduced Vt in both early and late segments. Hexamethylene-amiloride (HMA), a specific Na(+)-H+ exchange blocker, reduced JHCO3 in both segments (ED by 43.6 and LD by 40.3%) without affecting Vt. Benzamil, an Na(+)-channel blocker, reduced Vt by 75.9 in ED and 74.9% in LD but had no significant effect on acidification in both segments. The specific inhibitor of H(+)-ATPase, bafilomycin A1, inhibited LD JHCO3 at a concentration of 2 x 10(-7) M by 49%, but ED was inhibited by 24% only at 2 x 10(-6) M. Sch-28080, an inhibitor of gastric H(+)-K(+)-ATPase, reduced JHCO3 by 35% in LD of K(+)-depleted rats but not in control rats and had no effect on ED. These data indicate that, in ED, bicarbonate reabsorption is mediated mostly by Na(+)-H+ exchange. In LD, there is evidence for contribution of Na(+)-H+ exchange, vacuolar H(+)-ATPase, and H(+)-K(+)-ATPase (in K(+)-depleted rats) to bicarbonate reabsorption.

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