Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Abstract

Dua AK, Dua N, Murrant CL. Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency. Am J Physiol Heart Circ Physiol 297: H433-H442, 2009. First published May 22, 2009 doi:10.1152/ajpheart.00216.2009.-To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4,20, and 40 Hz;15 . L-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia. stimulus frequency; contraction frequency; arteriole; skeletal muscle contraction; active hyperemia BLOOD FLOW TO ACTIVE SKELETAL muscle increases during contraction. It is hypothesized that active skeletal muscle cell metabolites are a source of vasodilators that cause active hyperemia during contraction, but there is little consensus as to the identity of the vasodilators involved. A host of potential metabolic vasodilators such as adenosine (ADO), hydrogen ions, decreased oxygen tension, carbon dioxide, phosphate, etc., as well as a host of endothelial-derived products and products of muscle activation such as nitric oxide (NO), potassium (K ϩ ), prostaglandins, ACh, ATP-dependent K ϩ (K ATP ) channels, etc. (for review, see Refs. 6,18,28,36), have been implicated in the processes of active hyperemia, but there is a general lack of agreement as to the relative importance of each. We have been investigating the impact of stimulation parameters in the processes of arteriolar vasodilation during active hyperemia to understand this general lack of agreement. We surmised that if the dilators are proposed to be products of skeletal muscle activation or metabolism then it stands to reason that if activation or metabolism is changed through different stimulation parameters then the dilators being produced may also change. Thus, to understand the impact that stimulation parameters have on the production of different vasodilators in active hyperemia, we have investigated the effects of stimulation par...

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Relaxin induces rapid, transient vasodilation in the microcirculation of hamster skeletal muscle

“…Preparations were then superfused with known pharmacological inhibitors of NO synthase (N(G)-nitro-L-arginine methyl ester (L-NAME); 10 K5 M) (Murrant & Sarelius 2002, Dua et al 2009) or inhibitors of potassium channels, ATP-dependent potassium (K ATP ) channel inhibitor glibenclamide (GLIB; 10 K5 M) (Murrant & Sarelius 2002) or calcium-associated potassium (K Ca ) channel inhibitor iberiotoxin (IBTX; 10 K7 M) (Jackson & Blair 1998) or tetraethylammonium (TEA) (10 K3 M) (Jackson & Blair 1998). Experiments involving L-NAME application produced significant arteriolar vasoconstriction presumably due to the inhibition of endogenous NO production.…”