Angiotensin II maintains, but does not mediate, isoproterenol-induced cardiac hypertrophy in rats. 1994

E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.

The role of angiotensin II (ANG II) in the development of isoproterenol (Iso)-induced cardiac hypertrophy was examined in rats. Iso increased cardiac mass, left ventricular RNA-to-DNA ratio, and the cardiac content of both myosin heavy chain and hydroxyproline in a dose-dependent manner, indicating that Iso-induced cardiac hypertrophy involves growth of both muscle and connective tissue. Cardiac hypertrophy reverted within 11-14 days after cessation of Iso. Propranolol prevented development of Iso-induced cardiac hypertrophy but did not affect the rate of its reversal. The ANG II receptor blocker losartan (Los) did not significantly decrease the hypertrophic response to Iso. Los injected after cessation of Iso dramatically enhanced the reversal of cardiac hypertrophy, even in rats that received Los with Iso during the induction of Iso-induced cardiac hypertrophy. ANG II, injected continuously at a subpressor dose that did not affect heart weight when given alone, inhibited reversal of cardiac hypertrophy when given after cessation of Iso. Los did not significantly affect the induction of the protooncogene c-fos by Iso. We conclude that endogenous ANG II has a major function in maintaining Iso-induced cardiac hypertrophy but does not mediate its induction. This suggests that different interactive stimuli may be required for development of cardiac hypertrophy, i.e., for initiation and for maintenance.

UI MeSH Term Description Entries
D007093 Imidazoles Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
D007545 Isoproterenol Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant. Isoprenaline,Isopropylarterenol,4-(1-Hydroxy-2-((1-methylethyl)amino)ethyl)-1,2-benzenediol,Euspiran,Isadrin,Isadrine,Isopropyl Noradrenaline,Isopropylnoradrenaline,Isopropylnorepinephrine,Isoproterenol Hydrochloride,Isoproterenol Sulfate,Isuprel,Izadrin,Norisodrine,Novodrin,Hydrochloride, Isoproterenol,Noradrenaline, Isopropyl,Sulfate, Isoproterenol
D007741 Labetalol A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS. AH-5158,Albetol,Apo-Labetalol,Dilevalol,Labetalol Hydrochloride,Labetalol, (R,R)-Isomer,Labetolol,Normodyne,Presolol,R,R-Labetalol,SCH-19927,Trandate,AH 5158,AH5158,Apo Labetalol,ApoLabetalol,Hydrochloride, Labetalol,R,R Labetalol,SCH 19927,SCH19927
D008297 Male Males
D008750 Methyldopa An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent. Methyldopate,alpha-Methyldopa,Aldomet,Alphamethyldopa,Apo-Methyldopa,Dopamet,Dopegit,Dopegyt,Dopergit,Hydopa,Meldopa,Nu-Medopa,Sembrina,alpha-Methyl-L-Dopa,Apo Methyldopa,Nu Medopa,alpha Methyl L Dopa,alpha Methyldopa
D008969 Molecular Sequence Data Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories. Sequence Data, Molecular,Molecular Sequencing Data,Data, Molecular Sequence,Data, Molecular Sequencing,Sequencing Data, Molecular
D009206 Myocardium The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow. Muscle, Cardiac,Muscle, Heart,Cardiac Muscle,Myocardia,Cardiac Muscles,Heart Muscle,Heart Muscles,Muscles, Cardiac,Muscles, Heart
D009218 Myosins A diverse superfamily of proteins that function as translocating proteins. They share the common characteristics of being able to bind ACTINS and hydrolyze MgATP. Myosins generally consist of heavy chains which are involved in locomotion, and light chains which are involved in regulation. Within the structure of myosin heavy chain are three domains: the head, the neck and the tail. The head region of the heavy chain contains the actin binding domain and MgATPase domain which provides energy for locomotion. The neck region is involved in binding the light-chains. The tail region provides the anchoring point that maintains the position of the heavy chain. The superfamily of myosins is organized into structural classes based upon the type and arrangement of the subunits they contain. Myosin ATPase,ATPase, Actin-Activated,ATPase, Actomyosin,ATPase, Myosin,Actin-Activated ATPase,Actomyosin ATPase,Actomyosin Adenosinetriphosphatase,Adenosine Triphosphatase, Myosin,Adenosinetriphosphatase, Actomyosin,Adenosinetriphosphatase, Myosin,Myosin,Myosin Adenosinetriphosphatase,ATPase, Actin Activated,Actin Activated ATPase,Myosin Adenosine Triphosphatase
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
D002216 Captopril A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin. (S)-1-(3-Mercapto-2-methyl-1-oxopropyl)-L-proline,Capoten,Lopirin,SQ-14,225,SQ-14,534,SQ-14225,SQ-14534,SQ 14,225,SQ 14,534,SQ 14225,SQ 14534,SQ14,225,SQ14,534,SQ14225,SQ14534

Related Publications

E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
July 1994, The American journal of physiology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
January 1990, The American journal of cardiovascular pathology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
June 1992, Hypertension (Dallas, Tex. : 1979),
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
April 2003, Clinical and experimental pharmacology & physiology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
August 2005, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
September 2010, Journal of molecular and cellular cardiology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
May 2011, FASEB journal : official publication of the Federation of American Societies for Experimental Biology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
June 2009, The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
February 2023, Biology of the cell,
E Golomb, and Z A Abassi, and G Cuda, and M Stylianou, and V R Panchal, and D Trachewsky, and H R Keiser
August 2012, Canadian journal of physiology and pharmacology,
Copied contents to your clipboard!