Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O-2 transport in exercise

Citation
F. Favret et al., Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O-2 transport in exercise, AM J P-REG, 280(3), 2001, pp. R730-R738
Citations number
25
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
280
Issue
3
Year of publication
2001
Pages
R730 - R738
Database
ISI
SICI code
0363-6119(200103)280:3<R730:MAACRF>2.0.ZU;2-Z
Abstract
The time course of changes in rat myocardial alpha (1)- and beta -adrenocep tors and of muscarinic cholinergic (M-Ach) receptor characteristics was stu died parallel with the changes in exercise systemic O-2 transport during a 21-day period of hypoxia (barometric pressure 380 Torr) to assess the effec ts of receptor modification during acclimatization on maximal exercise capa city. Hypoxia resulted in polycythemia, pulmonary hypertension, right ventr icular hypertrophy, and transient left ventricular weight loss. Maximal O-2 consumption at 30 min of hypoxia was reduced to 60% of the normoxic value and remained unchanged. This was partly due to a gradual decrease in maxima l cardiac output and heart rate (HRmax), which offset the increase in blood O-2 content. HRmax correlated positively (r = 0.994) with beta -adrenocept or density and negatively (r = -0.964) with M-Ach-receptor density, suggest ing that HRmax reduction results from intrinsic changes in myocardial recep tor characteristics leading to reduced responses to adrenergic stimulation and elevated responses to cholinergic stimulation. alpha -Adrenoceptor dens ity in both ventricles increased initially to eventually fall below normoxi c values. The dissociation between the different patterns of right and left ventricular weight and the similar pattern of alpha -adrenoceptor change i n both ventricles do not support a role for these receptors on right ventri cular myocardial hypertrophy.