BIOMAT Database Logo BIOMAT Database Logo

Alterations in expression of sarcoplasmic reticulum gene in Dahl rats during the transition from compensatory myocardial hypertrophy to heart failure. 1997

H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Second Department of Internal Medicine, Ehime University School of Medicine, Japan.

OBJECTIVE To clarify whether the functional changes during the transition from compensatory myocardial hypertrophy to failure are associated with changes in sarcoplasmic reticulum gene expression. METHODS We examined the gene expression of sarcoplasmic reticulum proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, calsequestrin and ryanodine receptor] in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (8%) diet from the age of 6 weeks. In-vivo contractile functioning was evaluated using echocardiography, and gene expression of sarcoplasmic reticulum proteins in the left ventricle was analyzed by Northern blotting for each stage of left ventricular hypertrophy. RESULTS SERCA messenger RNA (mRNA) levels in Dahl-S rats with compensatory hypertrophy did not change significantly, whereas phospholamban mRNA levels were increased by 61% (P < 0.01), and calsequestrin mRNA levels were increased by 130% (P < 0.01) compared with those in Dahl salt-resistant (Dahl-R) rats. SERCA mRNA levels in Dahl-S rats with decompensated dilatation were decreased by 32% (P< 0.05), whereas levels of phospholamban and calsequestrin mRNA remained unchanged. Ryanodine receptor mRNA levels did not change either with compensatory hypertrophy or with decompensated dilatation. CONCLUSIONS Alterations in expression of sarcoplasmic reticulum gene may be related to changes in systolic and diastolic properties in compensatory hypertrophy and heart failure.

UI MeSH Term Description Entries
D009200 Myocardial Contraction Contractile activity of the MYOCARDIUM. Heart Contractility,Inotropism, Cardiac,Cardiac Inotropism,Cardiac Inotropisms,Contractilities, Heart,Contractility, Heart,Contraction, Myocardial,Contractions, Myocardial,Heart Contractilities,Inotropisms, Cardiac,Myocardial Contractions
D011919 Rats, Inbred Strains Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding. August Rats,Inbred Rat Strains,Inbred Strain of Rat,Inbred Strain of Rats,Inbred Strains of Rats,Rat, Inbred Strain,August Rat,Inbred Rat Strain,Inbred Strain Rat,Inbred Strain Rats,Inbred Strains Rat,Inbred Strains Rats,Rat Inbred Strain,Rat Inbred Strains,Rat Strain, Inbred,Rat Strains, Inbred,Rat, August,Rat, Inbred Strains,Rats Inbred Strain,Rats Inbred Strains,Rats, August,Rats, Inbred Strain,Strain Rat, Inbred,Strain Rats, Inbred,Strain, Inbred Rat,Strains, Inbred Rat
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D002135 Calcium-Binding Proteins Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS. Calcium Binding Protein,Calcium-Binding Protein,Calcium Binding Proteins,Binding Protein, Calcium,Binding Proteins, Calcium,Protein, Calcium Binding,Protein, Calcium-Binding
D002155 Calsequestrin Acidic protein found in SARCOPLASMIC RETICULUM that binds calcium to the extent of 700-900 nmoles/mg. It plays the role of sequestering calcium transported to the interior of the intracellular vesicle.
D004452 Echocardiography Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. Echocardiography, Contrast,Echocardiography, Cross-Sectional,Echocardiography, M-Mode,Echocardiography, Transthoracic,Echocardiography, Two-Dimensional,Transthoracic Echocardiography,2-D Echocardiography,2D Echocardiography,Contrast Echocardiography,Cross-Sectional Echocardiography,Echocardiography, 2-D,Echocardiography, 2D,M-Mode Echocardiography,Two-Dimensional Echocardiography,2 D Echocardiography,Cross Sectional Echocardiography,Echocardiography, 2 D,Echocardiography, Cross Sectional,Echocardiography, M Mode,Echocardiography, Two Dimensional,M Mode Echocardiography,Two Dimensional Echocardiography
D006332 Cardiomegaly Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES. Cardiac Hypertrophy,Enlarged Heart,Heart Hypertrophy,Heart Enlargement,Cardiac Hypertrophies,Enlargement, Heart,Heart Hypertrophies,Heart, Enlarged,Hypertrophies, Cardiac,Hypertrophies, Heart,Hypertrophy, Cardiac,Hypertrophy, Heart
D006333 Heart Failure A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION. Cardiac Failure,Heart Decompensation,Congestive Heart Failure,Heart Failure, Congestive,Heart Failure, Left-Sided,Heart Failure, Right-Sided,Left-Sided Heart Failure,Myocardial Failure,Right-Sided Heart Failure,Decompensation, Heart,Heart Failure, Left Sided,Heart Failure, Right Sided,Left Sided Heart Failure,Right Sided Heart Failure
D006352 Heart Ventricles The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation. Cardiac Ventricle,Cardiac Ventricles,Heart Ventricle,Left Ventricle,Right Ventricle,Left Ventricles,Right Ventricles,Ventricle, Cardiac,Ventricle, Heart,Ventricle, Left,Ventricle, Right,Ventricles, Cardiac,Ventricles, Heart,Ventricles, Left,Ventricles, Right
D000252 Calcium-Transporting ATPases Cation-transporting proteins that utilize the energy of ATP hydrolysis for the transport of CALCIUM. They differ from CALCIUM CHANNELS which allow calcium to pass through a membrane without the use of energy. ATPase, Calcium,Adenosinetriphosphatase, Calcium,Ca(2+)-Transporting ATPase,Calcium ATPase,Calcium Adenosinetriphosphatase,Adenosine Triphosphatase, Calcium,Ca2+ ATPase,Calcium-ATPase,ATPase, Ca2+,ATPases, Calcium-Transporting,Calcium Adenosine Triphosphatase,Calcium Transporting ATPases,Triphosphatase, Calcium Adenosine

Related Publications

H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Alterations in myosin heavy chain isoform gene expression during the transition from compensatory hypertrophy to congestive heart failure in rats.
February 2001, Chinese medical journal,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Mechanoenergetic alterations during the transition from cardiac hypertrophy to failure in Dahl salt-sensitive rats.
January 1998, Circulation,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Sarcoplasmic reticulum gene expression in cardiac hypertrophy and heart failure.
April 1994, Circulation research,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Transgenic expression of sarcoplasmic reticulum Ca(2+) atpase modifies the transition from hypertrophy to early heart failure.
August 2001, Circulation research,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Transition from compensatory hypertrophy to dilated, failing left ventricles in Dahl salt-sensitive rats.
December 1994, The American journal of physiology,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Hydrogen sulfide mitigates transition from compensatory hypertrophy to heart failure.
April 2011, Journal of applied physiology (Bethesda, Md. : 1985),
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Neurohumoral factors during transition from left ventricular hypertrophy to failure in Dahl salt-sensitive rats.
January 1995, Biochemical and biophysical research communications,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Transition from compensatory hypertrophy to dilated failing left ventricle in Dahl-Iwai salt-sensitive rats.
May 1997, American journal of hypertension,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Cardiac calcineurin during transition from hypertrophy to heart failure in rats.
June 2000, Biochemical and biophysical research communications,
H Okayama, and M Hamada, and H Kawakami, and S Ikeda, and H Hashida, and Y Shigematsu, and K Hiwada
Sarcoplasmic reticulum Ca2+ ATPase gene expression to the rescue of myocardial contractility in hypothyroid associated heart failure.
August 1999, Cardiovascular research,
Copied contents to your clipboard!