Abstract
beta-Adrenergic receptors (beta-AR) are essential regulators of cardiovascular
homeostasis. In addition to their prominent function in the heart,
beta-AR are located on vascular smooth muscle cells, where they mediate
vasodilating effects of endogenous catecholamines. In this study,
we have investigated in an isometric myograph different types of
blood vessels from mice lacking beta(1)- and/or beta(2)-adrenergic
receptor subtypes (beta(1)-KO, beta(2)-KO, beta(1)beta(2)-KO). In
wild-type mice, isoproterenol induced relaxation of segments from
thoracic aorta, carotid, femoral and pulmonary arteries, and portal
vein. The relaxant effect of beta-receptor stimulation was absent
in femoral and pulmonary arteries from beta(1)-KO mice. In aortic
and carotid arteries and in portal veins, the vasodilating effect
of isoproterenol was reduced in mice lacking beta(1)- or beta(2)-receptors.
However, in these vessels the vasodilating effect was only abolished
in double KO mice lacking both beta(1)- and beta(2)-receptors. Vessel
relaxation induced by forskolin did not differ between wild-type
and KO mice. Similar contributions of beta(1)- and beta(2)-receptors
to isoproterenol-induced vasorelaxation were found when vessels from
KO mice were compared with wild-type arteries in the presence of
subtype-selective beta-receptor antagonists. These studies demonstrate
that beta(1)-adrenergic receptors play a dominant role in the murine
vascular system to mediate vasodilation. Surprisingly, beta(2)-receptors
contribute to adrenergic vasodilation only in a few major blood vessels,
suggesting that differential distribution of beta-adrenergic receptor
subtypes may play an important role in redirection of tissue perfusion.
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