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Articles in PresS, published online ahead of print December 5, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00441.2002
Submitted on May 24, 2002
Accepted on November 25, 2002
1-adrenergic receptor (AR) responses in 1AB-AR knockout mouse hearts suggests presence of 1D-AR
1 Department of Radiology, University of California San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA; Department of Cardiology, Veterans Affairs Medical Center, San Francisco, CA, USA
2 Department of Radiology, University of California San Francisco, San Francisco, CA, USA; Department of Cardiology, Veterans Affairs Medical Center, San Francisco, CA, USA
3 Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA; Department of Cardiology, Veterans Affairs Medical Center, San Francisco, CA, USA
4 Department of Cardiology, Veterans Affairs Medical Center, San Francisco, CA, USA; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA; Department of Medicine, University of California San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: ajbaker{at}itsa.ucsf.edu.
Two functional 
1-adrenergic receptor (AR) subtypes (1A and 1B) have been identified in the mouse heart. However, it is unclear if the third known subtype, 1D-AR, is also present. To investigate this, we determined if there were 1-AR responses in hearts from a novel mouse model lacking 1A- and 1B-ARs (ABKO). In Langendorff-perfused hearts, 1-ARs were stimulated with phenylephrine. For ABKO hearts, phenylephrine reduced left ventricular pressure and coronary flow (to 87±2% and 86±4% of initial respectively, n=11, p<0.01). These effects were blocked by prazosin and BMY 7378, suggesting 1D-AR-mediated responses. In contrast, trabeculae from ABKO hearts did not respond to phenylephrine, suggesting that in ABKO perfused hearts the effects of phenylephrine were not mediated by direct actions on cardiomyocytes. A novel finding was that 1-AR stimulation caused positive inotropy in the wild type mouse heart in contrast to the negative inotropy observed in mouse cardiac muscle strips. We conclude that mouse hearts lacking 1A- and 1B-ARs retain functional 1-AR responses involving decreases of coronary flow and ventricular pressure that reflect 1D-AR-mediated vasoconstriction. Furthermore, 1-AR inotropic responses depend critically on the experimental conditions.
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