Caveolin-2 (Cav2) is a major protein component of caveolae in membranes of vascular smooth muscle and endothelium yet its absence alters the ultrastructure of skeletal muscle fibers. To gain insight into Cav2 function in skeletal muscle, we tested the hypothesis that genetic deletion of Cav2 would alter microvascular reactivity and depress contractile function of skeletal muscle in vivo. In the left gluteus maximus muscle (GM) of anesthetized Cav2-/- and wild-type (WT) male mice (age, 6 months), microvascular responses to physiological agonists and to GM contractions were studied at 35°C. For feed arteries (FA), first- (1A), second- (2A) and third-order (3A) arterioles, respective mean diameters at rest (45, 35, 25, 12 µm) and during maximal dilation (65, 55, 45, 30 µm) were similar between groups. Cumulative dilations to acetylcholine (ACh, 10-9-10-5M) and constrictions to norepinephrine (10-9-10-5 M) were also similar between groups, as were steady state dilations during rhythmic twitch contractions (2 and 4Hz; 30s). For single tetanic contractions (100Hz; 100, 250, 5 00ms), Rapid Onset Vasodilation (ROV) increased with contraction duration throughout networks in GM of both groups but was reduced by nearly half in Cav2-/- mice compared to WT mice (P<0.05). Nevertheless, maximal force during tetanic contraction was ~40% greater in GM of Cav2-/- vs. WT mice (152±14 vs. 110±3 mN per square millimeter, respectively; P<0.05) Thus, while structural and functional properties of resistance networks are well-maintained in the GM of Cav2-/- mice, diminished ROV with greater force production reveals novel physiological roles for Cav2 in skeletal muscle.
- blood flow
- feed artery
- Copyright © 2016, American Journal of Physiology - Heart and Circulatory Physiology