HYPERPOLARIZATION OF IN-SITU RAT SAPHENOUS-VEIN IN RESPONSE TO AXIAL STRETCH

The goal of this study was to measure the effect of axial stretch on v ascular smooth muscle (VSM) transmembrane potential (E(m)) and externa l diameter (D(e)) of intact and deendothelialized rat saphenous veins (SV). Incremental increases in length of SV were produced in situ by b iaxial stretch of its perivascular connective tissue. E(m) was measure d in situ with glass microelectrodes and D(e) with a high-resolution e yepiece or on-line video microangiometer. Vessels were locally denerva ted by 20 min superfusion with 6-hydroxydopamine. Endothelium was remo ved by maintaining an air bolus in the lumen for 6 min. Axial stretch of endothelium-intact SV from a baseline length (L0, at which there wa s no vessel buckling or folding) to 120% L0 induced a small depolariza tion from -56 +/- 1.2 to -53 +/- 0.8 mV. This was followed by a substa ntial hyperpolarization to -65 +/-1.4 mV at 140% L0. However, a depola rization was observed in deendothelialized SV from -47 +/- 1.3 mV at L 0 to -43 +/- 1.8 mV at 140% L0. Neither E(m) response was influenced b y local denervation. Relative to L0, 40% stretch also attenuated norep inephrine-induced vasoconstriction. These results suggest that axial s tretch of SV can lead to release of endothelium-derived factor(s) that hyperpolarizes venous VSM and possibly attenuates stretch-induced and adrenergic vasoconstriction. Such a response may act as a protective mechanism to attenuate vasoconstriction induced by axial stretch.