α‐Adrenergic inhibition increases collateral circuit conductance in rats following acute occlusion of the femoral artery

Abstract

This study evaluated whether α-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) α-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after α inhibition during the same treadmill speed. α 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. α 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 α 1 activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting α 2 receptors in the presence of α 1 inhibition increased (43 ± 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective α inhibition with phentolamine increased collateral conductance (242 ± 59%; P < 0.05). We interpret these findings to indicate that both α 1 -and α 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.

Chronic femoral artery occlusion augments exercise pressor reflex in decerebrated rats

“…At first glance, these findings contrast markedly with those in the cat and the human (1,4,8,16,21,33). One must realize, however, that, after femoral arterial ligation in our experiments, the residual blood flow capacity to the hindlimb muscles of the rat was still three times greater than the blood flow measured when these muscles were inactive (34). Consequently, the mismatch between blood supply and demand in either the 72-h or the 3-min occluded groups may not have been severe enough to evoke a pressor response during the postcontraction period.…”

“…The rats were allowed to recover 72 h before the experiments were started. Femoral artery occlusion has been reported to have no effect on normal cage activity (34).…”

Blockade of ATP-sensitive potassium channels prevents the attenuation of the exercise pressor reflex by tempol in rats with ligated femoral arteries

“…Second, ligation increased the amount of protein comprising part of the K ATP channel. The failure of ligation to decrease the two potassium channels is not too surprising because the procedure has been shown to provide adequate blood flow to the hindlimb of cage-restrained rats, making the likelihood of tissue injury low (40,50).…”

“…The rats were allowed to recover 72 h before the experiments were started. Femoral artery occlusion has been reported to have no effect on normal cage activity (40). This technique has been shown to reduce blood flow capacity to ϳ10 -20% of normal while having little effect on resting blood flow (29,49).…”

Alteration of the mu opioid receptor: Ca2+channel signaling pathway in a subset of rat sensory neurons following chronic femoral artery occlusion

“…Afterward, the wounds were closed with skin clips, and the animals were allowed to recover for 72 h before DRG isolation. Femoral artery occlusion has been reported to have no effect on normal cage activity (Taylor et al 2008). In this set of experiments, the freely perfused hindlimbs (right) served as controls.…”