Mechanical, electrical, and biochemical effects of hypoxia and substrate removal on spontaneously active vascular smooth muscle.
Effects of hypoxia and glucose-free solution on the isolated rat portal vein were studied. Decrease of extracellular PO2 below 50 mm Hg caused graded inhibition of spontaneous mechanical activity; below 7 mm Hg, inhibition was complete in most preparations. Contracture force of depolarized portal vein was less sensitive to decreases in PO2. Responses to noradrenaline at all concentrations were markedly depressed at extreme hypoxia. Sucrose-gap experiments showed that hypoxia reduced the spontaneous electrical spike discharge. Mean tissue contents of PCr, ATP and glycogen (expressed as glucose) were 3.02, 2.47 and 5.07 micromol/g cell wt. in spontaneously active control muscles and 1.07, 1.65 and 1.83 after 20 min anoxia. Physiological variations in PO2 may influence myogenic activity of vascular smooth muscle largely through an action at the membrane level and this mechanism may participate in local blood flow control. Caculations indicated that the graded response to hypoxia in the present in vitro experiments was not due to diffusion limitation. Spontaneous mechanical activity was relatively well maintained even after prolonged exposure to glucose-free solution, whereas the responses to K+ and noradrenaline were markedly suppressed. Electrophysiological recordings during spontaneous activity indicated desynchronization and impaired conduction. PCr and ATP were maintained at control levels and glycogen reduced by 50 per cent after 2 h in glucose-free medium. Indications of the use of amino acids (glutamate) as substrate under these conditions were obtained.
D000200:Action Potentials; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D008564:Membrane Potentials; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000378:metabolism / Q000503:physiopathology*; D010313:Partial Pressure; D010725:Phosphocreatine / Q000378:metabolism; D011169:Portal Vein / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006003:Glycogen; D005947:Glucose