Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange

Valentino Piacentino; Christopher R. Weber; John P. Gaughan; Kenneth B. Margulies; Donald M Bers; Steven R. Houser

Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange

Valentino Piacentino, Christopher R. Weber, John P. Gaughan, Kenneth B. Margulies, Donald M Bers, Steven R. Houser

Research output: Contribution to journal › Article › peer-review

Abstract

A decrease in the peak systolic [Ca]_i and slow decay of the Ca_i transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.

Original language	English (US)
Pages (from-to)	466-471
Number of pages	6
Journal	Annals of the New York Academy of Sciences
Volume	976
State	Published - 2002
Externally published	Yes

Keywords

Cardiac Na/Ca exchange
Contractility
Heart failure
Sarcoplasmic reticulum

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

Fingerprint Dive into the research topics of 'Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange'. Together they form a unique fingerprint.

Cite this

@article{7d61f21e5576487cb73ddc0893104de5,

title = "Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange",

abstract = "A decrease in the peak systolic [Ca]i and slow decay of the Cai transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.",

keywords = "Cardiac Na/Ca exchange, Contractility, Heart failure, Sarcoplasmic reticulum",

author = "Valentino Piacentino and Weber, {Christopher R.} and Gaughan, {John P.} and Margulies, {Kenneth B.} and Bers, {Donald M} and Houser, {Steven R.}",

year = "2002",

language = "English (US)",

volume = "976",

pages = "466--471",

journal = "Annals of the New York Academy of Sciences",

issn = "0077-8923",

publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange

AU - Piacentino, Valentino

AU - Weber, Christopher R.

AU - Gaughan, John P.

AU - Margulies, Kenneth B.

AU - Bers, Donald M

AU - Houser, Steven R.

PY - 2002

Y1 - 2002

N2 - A decrease in the peak systolic [Ca]i and slow decay of the Cai transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.

AB - A decrease in the peak systolic [Ca]i and slow decay of the Cai transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.

KW - Cardiac Na/Ca exchange

KW - Contractility

KW - Heart failure

KW - Sarcoplasmic reticulum

UR - http://www.scopus.com/inward/record.url?scp=0036969039&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036969039&partnerID=8YFLogxK

M3 - Article

C2 - 12502596

AN - SCOPUS:0036969039

VL - 976

SP - 466

EP - 471

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -

Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange

Abstract

Keywords

ASJC Scopus subject areas

Other files and links

Cite this