American Journal of Physiology-Heart and Circulatory Physiology · 1977 · 73 citations · 0 references
Life SciencesPharmacologyPhysiologyNeuropharmacologyNeurophysiologyPharmacodynamicsAutonomic Nervous SystemBlood Pressure RegulationCardiovascular PhysiologyCirculatory PhysiologyHemodynamicsNorepinephrine SignalingRecordingsSympathetic ActivationSympathetic Vasomotor ControlVascular Smooth Muscle PharmacologyVascular Smooth Muscle RegulationVascular Smooth Muscle RelaxationVasoconstrictive Neurotransmission
Helical strips from arteries with a rich sympathetic innervation (rat tail and femoral, and dog mesenteric arteries) develop a sustained contracture when exposed to a K-free physiological salt solution (PSS). The contracture can be blocked by phentolamine and does not occur in arteries whose nerve terminals have been destroyed with 6-hydroxydopamine. The temporal relationship between force development and efflux of NE was determined. Helical strips of rat tail arteries or dog mesenteric arteries were incubated in PSS containing 1-norepinephrine-7-3H([3H]NE). They were then transferred to a superfusion system which allowed isometric recordings and collection of the superfusate for the estimation of [3H]NE content. Following exposure to a K-free PSS force development paralleled NE release and both parameters were potentiated by ouabain. These data demonstrate that this neurogenic mechanism plays a most important role in the K-free contracture of the vascular smooth muscle studied. It is in accord with the observation that NE is released by adrenergic nerves following inhibition of Na+-K+-ATPase.