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Hypertension. 2005;45:e20-e21
Published online before print May 16, 2005, doi: 10.1161/01.HYP.0000167153.83102.15
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(Hypertension. 2005;45:e20.)
© 2005 American Heart Association, Inc.


Hypertension Electronic Pages

The Role of the {alpha}1B-Adrenergic Receptor in Vascular Structure and Function

Craig J. Daly; Ian McGrath

Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, Scotland


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

Townsend et al1 provide interesting subplots to the perplexing issue of the role of {alpha}1B-adrenoceptors (ARs) in cardiovascular regulation.

The physiological roles of this receptor are unclear because it has no universally acknowledged selective antagonists. This accentuates use of the {alpha}1B-knockout (KO) mouse2 and raises 2 sets of issues: (1) tissue distribution, and (2) developmental compensation.

First, Townsend et al’s interpretation of the attenuation found in the baroreceptor reflex of the {alpha}1B-KO mouse does not take account of the widespread distribution of the receptor in the central nervous system related to autonomic regulation. There is no more evidence for the loss of reflex being at the level of the heart than in the brain. Indeed, the statistically significant loss of the heart rate reflex would support the latter (admittedly, numerically trivial because heart rate is already maximal). More significant, if the cardiac role of {alpha}1B"is likely to be modest and secondary to ß-ARs," perhaps this also suggests that the heart is not the site of this action.

Second, the lack of selective antagonists limits interpretation of vascular phenotypes of the {alpha}1B-KO mouse. This strain does not show substantial changes from normal across a range of different arteries.3 In all arteries tested, there were subtle changes in the pharmacological data indicating that loss of {alpha}1B-AR changed the properties of the other receptors. In the small mesenteric arteries used by Townsend et al, antagonists indicate mainly {alpha}1A-AR in contraction. However, in the {alpha}1B-KO mouse, this vessel loses the ability . . . [Full Text of this Article]

Seth Townsend; Dan E. Berkowitz

Johns Hopkins Medical Institutions, Baltimore, Maryland