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J Physiol Volume 586, Number 6, 1649-1667, March 15, 2008 DOI: 10.1113/jphysiol.2007.149567
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CARDIOVASCULAR

{alpha}-Adrenergic inhibition increases collateral circuit conductance in rats following acute occlusion of the femoral artery

 Jessica C. Taylor1, Zeyi Li1, H. T. Yang1, M. Harold Laughlin1,2,3 and Ronald L. Terjung1,2,3

1 Department of Biomedical Sciences, College of Veterinary Medicine
2 Department of Medical Pharmacology and Physiology, College of Medicine
3 Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA

This study evaluated whether {alpha}-adrenergic activation contributes to collateral circuit vascular resistance in the hindlimb following acute unilateral occlusion of the femoral artery in rats. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced (15–35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) {alpha}-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after {alpha} inhibition during the same treadmill speed. {alpha}1 inhibition increased blood flow by ~40% to active muscles that were not affected by femoral occlusion, whereas collateral-dependent BFs to the calf muscles were reduced by 29 ± 8.4% (P < 0.05), due to a decrease in muscle conductance with no change in collateral circuit conductance. {alpha}2 inhibition decreased both collateral circuit (39 ± 6.0%; P < 0.05) and calf muscle conductance (36 ± 7.3%; P < 0.05), probably due to residual {alpha}1 activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting {alpha}2 receptors in the presence of {alpha}1 inhibition increased (43 ± 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective {alpha} inhibition with phentolamine increased collateral conductance (242 ± 59%; P < 0.05). We interpret these findings to indicate that both {alpha}1- and {alpha}2-receptor activation can influence collateral circuit resistance in vivo during the high flow demands caused by exercise. Furthermore, we observed a reduced maximal conductances of active muscles that were ischaemic. Our findings imply that in the presence of excessive sympathetic activation, which can occur in the condition of intermittent claudication during exertion, an exaggerated vasoconstriction of the existing collateral circuit and active muscle will occur.

(Received 8 December 2007; accepted after revision 17 January 2008; first published online 24 January 2008)
Corresponding author R. L. Terjung: Department of Biomedical Sciences, E102 Vet. Medical Bldg, University of Missouri, Columbia, MO 65211, USA. Email: terjungr{at}missouri.edu






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