Resistance to pressure-induced dilatation in femoral but not saphenous artery: physiological role of latch?

We recently determined that the ability of the femoral artery (FA) to maintain higher levels of tonic isometric stress compared with the saphenous artery (SA) was due to differential expression of motor proteins permitting latch-bridge formation in FA and not SA. Arteries under pressure in vivo are not constrained to contract isometrically. Thus the significance of latch-bridge formation in arterial physiology remains to be determined. To address this translational question, diameter changes of pressurized FA and SA were compared. The reduction in lumen diameter induced by KCl at 80 mmHg (isobaric active constriction; IAC) was greater at 30 s than 10 min in SA. In FA, the reverse was true, mimicking isometric contractile responses identified in our earlier work. From 80 to 150 mmHg, the %IAC induced by KCl was greater in SA than FA (e.g., approximately 80% vs. approximately 30% at 120 mmHg). This was not explained by differences in contractile mechanisms but was likely due to differences in absolute artery diameters. In constricted arteries subjected to a ramp increase in pressure from 60 to 120 mmHg, the constricted diameter of FA, but not SA, was greater than the IAC diameter at each pressure. Thus FA but not SA could maintain a smaller diameter on being pressurized when first constricted than it could achieve by isobaric constriction. These data support the hypothesis that latch bridges permit constricted large-diameter elastic arteries such as the FA to temporarily resist dilatation in the face of transient increases in blood pressures.