Review: reticuloruminal motility--a pharmacological target with a difference?

The vagal sensory inputs to and motor outputs from the hindbrain gastric centres required for reticuloruminal motility were sampled directly in anaesthetized sheep using electrophysiological 'single fibre' techniques and indirectly in conscious, surgically prepared sheep. Drugs were administered by close-arterial injection into a carotid artery to observe central effects and into the coeliac artery to observe peripheral effects on the reticulorumen. Escherichia coli lipopolysaccharide produced intermediates responsible for the smooth muscle relaxation in the first phase of reticuloruminal stasis and for gastric centre depression in the second phase. Adrenergic influences on reticuloruminal motility comprise (a) an alpha1 adrenoreceptor-induced contracture and raised tension receptor sensitivity, (b) an alpha2 adrenoreceptor-mediated depression of the gastric centres causing stasis, excitation of epithelial receptors evoking rumination, and interference with acetylcholine release in the parasympathetic pathway, (c) abeta1 adrenoreceptor-mediated inhibition of the gastric centres, and (d) abeta2 adrenoreceptor-mediated inhibition of intrinsic and extrinsic motility.