Modification of vagal depressor reflex by CO2 in spontaneously breathing rabbits.
The control of hindlimb and renal vascular beds by vagal afferents was studied, in anesthetized spontaneously breathing rabbits in which the carotid sinus and aortic depressor nerves were cut, by measuring the increase in vascular resistance (constant-flow perfusion with autologous blood) during bilateral vagal cold block (VCB). The effect of hypercapnia was studied with both increased ventilation (caused by inspiration of mixtures of CO2 in O2) and decreased ventilation (caused by infusion of gallamine during O2 breathing). The increase in hindlimb resistance with VCB was correlated with respiratory minute volume but not with PCO2; the reverse was true for the increase in renal resistance. Without VCB the renal vessel constriction caused by the hypercapnia was markedly attenuated, provided that there were minimal respiratory movements; the resistance increased dramatically when these movements were abolished or with VCB. Thus, the powerful central effect of CO2 on the renal vessels can be counteracted by vagal afferents activated by lung movement; even minimal respiratory activity can cause this effect.
D000818:Animals; D001011:Aorta / Q000294:innervation; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002346:Carotid Sinus / Q000294:innervation; D003250:Constriction; D006935:Hypercapnia; D007668:Kidney / Q000098:blood supply; D009132:Muscles / Q000098:blood supply; D009475:Neurons, Afferent / Q000502:physiology; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D011817:Rabbits / Q000502:physiology*; D012018:Reflex; D012039:Regional Blood Flow; D012119:Respiration; D014630:Vagus Nerve / Q000502:physiology*; D014655:Vascular Resistance
D002245:Carbon Dioxide