suggest that modification of LCC by H2O2 is not through the

PKA pathway, but through PKC, especially through PKCE

pathway.

Keywords: L-type calcium channel; Hydrogen peroxide;

Protein kinase C

doi:10.1016/j.yjmcc.2006.08.052

Y-D-2. B-Estradiol modulates expression and kinetics of

low-voltage activated CaV3.2 T-type Ca2+ channel

Farzana Marni, Tomoko Uchino, Mingqi Zheng, Yan Wang,

Shojiro Isomoto, Katsushige Ono. Oita University, Department

of Cardiovascular Science, Yufu, Oita 879-5593, Japan

Background: A biologically active estrogen h-estradiol is akey regulator of growth, differentiation, and function in a wide

array of cells and tissues, including cardiovascular systems.

Objective: The study was aimed to investigate the mechan-

isms of short-term and long-term effects of h-estradiol on the ionchannel expression focusing on the T-type Ca2+ channels.

Methods: Recombinant Cav3.1 (a1G) and Cav3.2 (a1H)

T-type Ca2+ channels were transfected into HEK 293 cells,

which were incubated in culture medium for 24 h with or

without h-estradiol. T-type Ca2+ channel currents were recordedusing a conventional whole-cell patch clamp method.

Results: h-Estradiol inhibits the expression of Cav3.2 T-

type Ca2+ channel in a dose-dependent manner (0.1–100 nM)

both in short-term (6–10 min) and long-term (24 h) effects; 10

nM h-estradiol decreased the maximum peak current of Cav3.2

channels by 8.5T0.6% (short-term) and 52.3% (long-term).

Steady-state inactivation and activation curves were signifi-

cantly shifted in the depolarized potential by short-term and

long-term treatments of h-estradiol. Whereas no significant

change was observed in the Cav3.1 channels by h-estradiol.Conclusion: h-Estradiol, a steroid hormone, modifies the

expression and the kinetics of the Cav3.2 channel but not the

Cav3.1 channel in the heterologous expression system.

Keywords: T-type Ca2+ channel; Estrogen; Remodeling

doi:10.1016/j.yjmcc.2006.08.053

Y-D-3. Non-genomic effects of aldosterone on intracellular

ion regulation and cell function in rat cardiomyocytes

Saori Matsui, Hiroshi Satoh, Hirotaka Kawashima, Shiro

Nagasaka, Chen Fung Niu, Tsuyoshi Urushida, Hideki Katoh,

Yasuhide Watanabe*, Hideharu Hayashi. Division of

Cardiology, Internal Medicine III, Hamamatsu University

School of Medicine, Japan. *Department of Basic Nursing,

Hamamatsu University School of Medicine, Japan

Background: Aldosterone has non-genomic effects that

express within minutes and modulate intracellular ion milieu

and cellular function. Recent studies have shown that

aldosterone activates Na+-K+-2Cl� co-transporter (NKCCl)

and/or Na+/H+ exchanger (NHE), which modify myocardial

contractility. However, it is still undefined whether aldosterone

actually alters intracellular ion concentrations or myocardial

contractility. To clarify the non-genomic effects of aldosterone,

we measured [Na+]i, Ca2+ transients (CaT), cell shortening

(CS) and cell volume in rat cardiomyocytes, and also evaluated

myocardial contractility.

Methods: Isolated myocytes were loaded with sodium

green (SG; 10 Amol/L), fluo-3/AM (10 Amol/L) and calcein/

AM (5 Amol/L) for 30 min for the measurements of [Na+]i,

[Ca2+]i and cell volume. The fluorescence images were

analyzed with a laser scanning confocal microscopy (LSCM)

at the room temperature.

Results: (1) Aldosterone increased the fluorescence inten-

sity of SG in a concentration-dependent manner and the

intensity reached 107T2% of the baseline at the concentration

of 100 nM within 5 min (meanTSE, n =8, p <0.05). (2)

Aldosterone up to 10 Amol/L did not alter CaT and CS in

isolated myocytes, developed tension in papillary muscles or

left ventricular developed pressure in Langendorff-perfused

hearts. (3) Aldosterone (100 nmol/L) increased the cell volume

from 43.8T2.6 pL to 45.9T2.7 pL (n =8, p <0.05). (4) Both the

increases in [Na+]i and cell volume were blocked by

bumetanide, an inhibitor of NKCC1, or by 5-(N-ethyl-N-

isopropyl) amiloride, an inhibitor of NHE.

Conclusion: Aldosterone rapidly increased [Na+]i and cell

volume via NKCC1 and NHE, whereas there was no change in

CaT or myocardial contractility. We conclude that the non-

genomic effects of aldosterone may be related to cell swelling

rather than to the increase in contractility.

Keywords: Aldosterone; Cell volume; Sodium

doi:10.1016/j.yjmcc.2006.08.054

Y-D-4. Altered expression of connexin43 contributes to the

arrhythmogenic substrate in early stage heart failure of

cardiomyopathic hamster

Takashi Sato, Tomoko Ohkusa, Haruo Honjo*, Shinsuke

Suzuki, Yuko Ishiguro*, Harumichi Nakagawa*, Masatoshi

Yamazaki*, Masafumi Yano, Itsuo Kodama*, Masunori

Matsuzaki. Division of Cardiology, Department of Medicine

and Clinical Science, Yamaguchi University Graduate School

of Medicine, Japan. *Research Institute of Environmental

Medicine, Nagoya University, Japan

The aim of this study was to clarify the connexin43 (Cx43)

gap junction remodeling and its potential role in the pathogen-

esis of arrhythmias during the development of heart failure.

Heart failure is known to predispose life-threatening ventricular

tachyarrhythmias even before compromising the systemic

circulation, but the underlying mechanism is not well

understood. We investigated stage-dependent changes in

Cx43 expression and associated alterations in the electrophy-

siological properties and propensities for life-threatening

ABSTRACTS / Journal of Molecular and Cellular Cardiology 41 (2006) 1039–10791052