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Articles in PresS, published online ahead of print November 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00610.2002
Submitted on July 16, 2002
Accepted on November 12, 2002
1 Department of Sports Medicine, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto, Nagano, Japan
2 Department of Molecular Oncology and Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto, Nagano, Japan
* To whom correspondence should be addressed. E-mail: nosehir{at}sch.md.shinshu-u.ac.jp.
Calponin is known as an actin binding protein in vascular smooth muscle that modifies contractile responses. However, its role in arterial pressure regulation has not been clarified. To assess this, mean arterial pressure (MAP) and heart rate (HR) were measured in calponin knockout (KO) mice and the results were compared with those in wild-type (WT) mice. The measurements were performed every 100 msec during a 60-min free-moving state each day for 3 days.
Mice in both groups rested during ~ 70% of the total measuring period. The mean HR during rest was significantly lower in KO mice than in WT mice but with no significant difference in MAP between the groups. HR response (
HR) to spontaneous change in MAP (MAP) varied in a wider range in KO mice with an 80% increase in the coefficient of variation for HR (P<0.05), while MAP in KO mice was controlled in a narrow range similar to that in WT mice. The baroreflex-sensitivity (HR/MAP), determined from the change in HR to the spontaneous change in MAP, was twofold higher in KO mice than that in WT mice (P<0.01), whereas there were no significant differences in the baroreflex-sensitivity determined by intravascular administration of phenylephrine and sodium-nitroprusside between the two groups (P>0.1). The MAP response to the administrated doses of phenylephrine in KO mice was reduced to one half of that in WT mice (P<0.01) but with no significant difference in the response to sodium-nitroprusside between the groups. The differences in HR variability and the spontaneous baroreflex-sensitivity between the two groups completely disappeared after carotid sinus denervation.
These results suggest that the higher variability in HR for KO mice was caused by the increased spontaneous arterial baroreflex-sensitivity, though not detected by the intravenous administration of the drug, and that the higher variability of HR may be a compensatory adaptation to the blunted 
-adrenergic response of peripheral vessels to sympathetic nervous activity.
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