|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION
1Heart Research Center, 2Department of Physiology and Pharmacology, 3School of Medicine (Cardiovascular Medicine), Oregon Health and Science University and 4Portland Veterans Affairs Medical Center, Portland, Oregon
Submitted 11 July 2006 ; accepted in final form 21 September 2006
While the fetal heart grows by myocyte enlargement and proliferation, myocytes lose their capacity for proliferation in the perinatal period after terminal differentiation. The relationship between myocyte enlargement, proliferation, and terminal differentiation has not been studied under conditions of combined arterial and venous hypertension, as occurs in some clinical conditions. We hypothesize that fetal arterial and venous hypertension initially leads to cardiomyocyte proliferation, followed by myocyte enlargement. Two groups of fetal sheep received intravascular plasma infusions for 4 or 8 days (from 130 days gestation) to increase vascular pressures. Fetal hearts were arrested in diastole and dissociated. Myocyte size, terminal differentiation (%binucleation), and cell cycle activity (Ki-67[+] cells as a % of mononucleated myocytes) were measured. We found that chronic plasma infusion greatly increased venous and arterial pressures. Heart (but not body) weights were
30% greater in hypertensive fetuses than controls. The incidence of cell cycle activity doubled in hypertensive fetuses compared with controls. After 4 days of hypertension, myocytes were (
11%) longer, but only after 8 days were they wider (
12%). After 8 days, %binucleation was
50% greater in hypertensive fetuses. We observed two phases of cardiomyocyte growth and maturation in response to fetal arterial and venous hypertension. In the early phase, the incidence of cell cycle activity increased and myocytes elongated. In the later phase, the incidence of cell cycle activity remained elevated, %binucleation increased, and cross sections were greater. This study highlights unique fetal adaptations of the myocardium and the importance of experimental duration when interpreting fetal cardiac growth data.
hypertrophy; hyperplasia; terminal differentiation; cardiomyocyte
This article has been cited by other articles:
![]() |
R. B. Sekar, E. Kizana, R. R. Smith, A. S. Barth, Y. Zhang, E. Marban, and L. Tung Lentiviral vector-mediated expression of GFP or Kir2.1 alters the electrophysiology of neonatal rat ventricular myocytes without inducing cytotoxicity Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2757 - H2770. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. L. Morrison, K. J. Botting, J. L. Dyer, S. J. Williams, K. L. Thornburg, and I. C. McMillen Restriction of placental function alters heart development in the sheep fetus Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R306 - R313. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |