Contraction-independent effects of catecholamines on glucose
transport in isolated rat cardiomyocytes.
Fischer, Y., J. Thomas, G. D. Holman, H. Rose, and H. Kammermeier.
Institute of Physiology, Medical Faculty, RWTH Aachen, Pauwelsstr.
30, D-52057 Aachen, Germany, Solvay Deutschland GmbH, PH-FEBK1, Hans
-B[diaeresis]ockler-Allee 20, D-30173 Hannover, Germany, Dept. of
Biochemistry, University of Bath, Claverton Down, Bath BA2 7AY,
U.K.
APStracts 2:0389C, 1995.
The effects of catecholamines on glucose transport were studied in
quiescent i.e. non-contracting cardiomyocytes isolated from adults
rats. [alpha]-Adrenergic treatment (100?[mu]M phenylephrine, or
100?[mu]M noradrenaline + 10?[mu]M propranolol) led to a ?4-fold
stimulation of 2-deoxy-D-glucose transport in basal cells (no
insulin). The effect of phenylephrine was suppressed by the [alpha]1
-adrenoreceptor antagonist prazosin, but was not affected by the
[alpha]2-antagonist yohimbine, nor by the -antagonist propranolol.
Exposure to the -adrenergic agonist isoprenaline (1?[mu]M) had no
stimulatory action on basal glucose transport, and even partially
counteracted the effect of phenylephrine (but not that of insulin).
The phenylephrine-induced rise in glucose transport occurred in two
phases with apparent half-times of 3.2?+/-?0.2 and 13.0?+/-?1.4?min,
respectively. Correspondingly, different EC50 values were found after
10 and 45?min upon phenylephrine addition (5.0?+/-?1.9 [mu]M vs.
31.6?+/-?9.6?[mu]M, resp.; p?=?0.002). Under maximally stimulating
conditions, phenylephrine's effect was at least partially additive to
that of insulin, and of other stimulators of glucose transport such
as phenylarsine oxide, hydrogen peroxide, vanadate, serotonin,
phorbol 12-myristate 13-acetate, lithium, and metformin.
Phenylephrine significantly increased the level of cell-surface
glucose carriers GLUT1 1.54-fold (p<0.001 vs. control), and
GLUT4 1.78-fold (p<0.01), as assessed by using the specific
photolabel 2-N-[4(1-azi-2,2,2-trifluoroethyl)benzoyl]-1,3-bis-(D
-mannos-4-yloxy)propyl-2-amine. In conclusion, catecholamines induce
an increase in cardiomyocyte glucose transport through 1-adrenergic
receptors independently or downstream of a contraction-evoked
stimulus. This effect is at least in part explained by a recruitment
of glucose transporters GLUT1 and GLUT4 to the cell surface. The
mechanism(s) and/or signals involved differ from those triggered by
insulin and insulinomimetic agents.
Received 24 July 1995; accepted in final form 17 October 1995.
APS Manuscript Number C449-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95