PMID- 8160826
OWN - NLM
STAT- MEDLINE
DCOM- 19940519
LR  - 20191210
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 266
IP  - 3 Pt 2
DP  - 1994 Mar
TI  - Cardiac hypertrophy in the ferret increases expression of the Na(+)-K(+)-ATPase 
      alpha 1- but not alpha 3-isoform.
PG  - H1221-7
AB  - Work overload alters expression of the Na(+)-K(+)-adenosinetriphosphatase 
      (ATPase) multigene family in the myocardium. However, due to lack of an 
      appropriate animal model, very little is known regarding regulation of the alpha 
      3-isoform. We previously reported that adult ferret myocardium expresses the 
      alpha 1- and alpha 3-isoforms of Na(+)-K(+)-ATPase. In the current study we 
      examined the relative abundances of these isoforms in a recently developed ferret 
      model of pressure-overload cardiac hypertrophy. Ferrets with abdominal aortic 
      constriction (Coarc) developed significant left ventricular hypertrophy based on 
      altered morphometric measurements and switching of the myosin heavy chain 
      isoforms. Western and Northern blotting analyses showed that in hypertrophied 
      left ventricles of Coarc ferrets the abundance of alpha 1-protein increased 
      (27%), whereas that of alpha 1-mRNA remained unchanged. In nonhypertrophied right 
      ventricles of Coarc ferrets abundance of alpha 1-protein remained unchanged. 
      Expression of the alpha 3-isoform in left ventricles of Coarc ferrets remained 
      unchanged at both protein and mRNA levels. By contrast, abundance of beta 1-mRNA 
      increased significantly (31%), whereas beta 1-protein remained unchanged. 
      Na(+)-K(+)-ATPase activity, estimated by K(+)-dependent nitrophenyl phosphatase 
      activity, did not differ between left ventricular homogenates from Coarc and 
      sham-operated ferrets. In conclusion, these studies indicate that in 
      hypertrophied ferret heart Na(+)-K(+)-ATPase isoforms are differentially 
      regulated at pretranslational, as well as at translational-posttranslational 
      levels.
FAU - Book, C B
AU  - Book CB
AD  - Department of Pharmacology, College of Medicine, Pennsylvania State University, 
      Hershey 17033.
FAU - Wilson, R P
AU  - Wilson RP
FAU - Ng, Y C
AU  - Ng YC
LA  - eng
GR  - HL-39723/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (DNA, Complementary)
RN  - 0 (Isoenzymes)
RN  - 0 (RNA, Messenger)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
SB  - IM
MH  - Animals
MH  - Aorta, Abdominal
MH  - Cardiomegaly/*metabolism
MH  - Constriction, Pathologic
MH  - DNA, Complementary/genetics
MH  - Ferrets
MH  - Isoenzymes/genetics/*metabolism
MH  - Male
MH  - Myocardium/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Sodium-Potassium-Exchanging ATPase/chemistry/genetics/*metabolism
MH  - Species Specificity
EDAT- 1994/03/01 00:00
MHDA- 1994/03/01 00:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 1994/03/01 00:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1152/ajpheart.1994.266.3.H1221 [doi]
PST - ppublish
SO  - Am J Physiol. 1994 Mar;266(3 Pt 2):H1221-7. doi: 
      10.1152/ajpheart.1994.266.3.H1221.