Vascular Tone and Ca2+ Signaling in Murine Cremaster Muscle Arterioles In Vivo


Address for Correspondence: Withrow G. Wier, Department of Physiology, University of Maryland Baltimore, Rm 525A Howard Hall, 660 West Redwood St., Baltimore, MD 21201 USA. E-mail:



We sought to determine some of the molecular requirements for basal state “tone” of skeletal muscle arterioles in vivo, and whether asynchronous Ca2+ waves are involved or not.


Cremaster muscles of anesthetized exMLCK and smGCaMP2 biosensor mice were exteriorized, and the fluorescent arterioles were visualized with wide-field, confocal or multiphoton microscopy to observe Ca2+ signaling and arteriolar diameter.


Basal state tone of the arterioles was ~50%. Local block of Ang-II receptors (AT1) or α1-adrenoceptors (α1-AR) had no effect on diameter, nor did complete block of sympathetic nerve activity (SNA). Inhibition of phospholipase C caused dilation nearly to the Ca2+-free (passive) diameter, as did exposure to nifedipine or 2-APB. Arterioles were also dilated when treated with SKF96365. High-resolution imaging of exMLCK fluorescence (ratio) or GCaMP2 fluorescence in smooth muscle cells failed to reveal Ca2+ waves (although Ca2+ waves/transients were readily detected by both biosensors in small arteries, ex vivo).


Arterioles of cremaster muscle have vascular tone of ~ 50%, which is not due to α1-AR, AT1R, or SNA. PLC activity, L-type Ca2+ channels, 2-APB- and SKF96365-sensitive channels are required. Propagating Ca2+ waves are not present. A key role for PLC and InsP3R in vascular tone in vivo, other than producing Ca2+ waves, is suggested.