Submitted on February 1, 2007
Accepted on June 5, 2007
Impact of 
1-adrenoceptor expression on contractile properties of vascular smooth muscle cells
Adrian Gericke1*, Peter Martinka1, Irina Nazarenko2, Pontus B. Persson3, and Andreas Patzak4
1 Institute of Vegetative Physiology, Humboldt-University of Berlin, Berlin, Berlin, Germany
2 Institute of Pathology, Humboldt-University of Berlin, Berlin, Berlin, Germany
3 Institute of Physiology, Humboldt University of Berlin, Berlin, Germany
4 Institute of Vegetative Physiology, Humboldt-University of Berlin, Berlin, Germany
* To whom correspondence should be addressed. E-mail: adrian.gericke{at}gmx.net.
Low-frequency blood pressure oscillations (Mayer waves) are discussed as a marker for sympathetic modulation of vascular tone. However, the factors that determine the frequency response of the vasculature to sympathetic stimuli are not fully understood. Possible mechanisms include functions related to 
1-adrenergic receptors (1-ARs) and post-receptor processes involved in the vascular contractile response. The purpose of the present study was to examine the hypothesis that expression levels of 1-ARs and their subtype distribution determine velocity and magnitude of 1-AR-mediated vascular smooth muscle cell (VSMC) contraction.
1-, 1B- and 1D-AR subtypes were transfected into VSMCs from rat aorta and characterized immunocytochemically via confocal microscopy. Functional studies in isolated cells were performed using video microscopy. The 1-AR agonist phenylephrine produced dose-dependent contractions of VSMCs. All transfected groups were more sensitive to phenylephrine compared with controls. Maximal contraction velocity almost doubled in transfected cells. However, no differences in observed parameters were found between the three transfected groups. Contractile properties in response to membrane depolarization with KCl were similar in all groups.
In conclusion, 1-AR density determines velocity and sensitivity of 1-AR-mediated contraction in VSMCs. 1-AR subtype distribution does not appear to influence vasoconstriction to sympathetic stimuli.
