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 vascular smooth muscle (VSM) transmembrane potential (Em) and external diameter (De) of intact and deendothelialized rat saphenous veins (SV). Incremental increases in length of SV were produced in situ by biaxial stretch of its perivascular connective tissue. Em was measured in situ with glass microelectrodes and De with a high-resolution eyepiece or on-line video microangiometer. Vessels were locally denervated by 20 min superfusion with 6-hydroxydopamine. Endothelium was removed by maintaining an air bolus in the lumen for 6 min. Axial stretch of endothelium-intact SV from a baseline length (Lo, at which there was no vessel buckling or folding) to 120% Lo induced a small depolarization from -56 +/- 1.2 to -53 +/- 0.8 mV. This was followed by a substantial hyperpolarization to -65 +/- 1.4 mV at 140% Lo. However, a depolarization was observed in deendothelialized SV from -47 +/- 1.3 mV at Lo to -43 +/- 1.8 mV at 140% Lo. Neither Em response was influenced by local denervation. Relative to Lo, 40% stretch also attenuated norepinephrine-induced vasoconstriction. These results suggest that axial stretch 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.