Mechanisms by which histamine stimulates rapidly adapting receptors in dog lungs.
The stimulant effect of histamine on intrapulmonary rapidly adapting receptors was studied in anesthetized, paralyzed, artificially ventilated dogs, to determine whether it was dependent on contraction of airway smooth muscle. Single- or few-afferent fiber recordings were made from small strands dissected from the otherwise intact vagus nerve. Aerosols of histamine increased both receptor discharge and tracheal pressure (Pt). In 27 experiments, isoproterenol prevented the increase in Pt but not in receptor activity induced by histamine. In another 32 experiments, acetylcholine (ACh) increased Pt to a greater extent than did histamine, whereas histamine increased receptor discharge more than ACh. When given as aerosol directly to the vicinity of the sensory receptor via a fiber bronchoscope, histamine stimulated 12 receptors, whereas ACh and buffer solution did not. Isoproterenol reduced slightly the stimulant effect of locally applied histamine on 8 receptors. We conclude that smooth muscle contraction is not essential for stimulant effects of histamine on rapidly adapting receptors in dog lungs, and that histamine acts directly on the receptors to increase their activity.
D000109:Acetylcholine / Q000494:pharmacology; D000336:Aerosols; D000818:Animals; D004285:Dogs; D006632:Histamine / Q000494:pharmacology*; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000294:innervation*; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000502:physiology; D012018:Reflex; D011984:Sensory Receptor Cells / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
D000336:Aerosols; D006632:Histamine; D007545:Isoproterenol; D000109:Acetylcholine