Reflex Inhibition of Intestinal Motility

Abstract

SINCE the classical study of intestinal motility by Bayliss and Starling¹ it has been generally assumed that the parasympathetic and the sympathetic components of the autonomic nervous system exert a central, reciprocal control of the activity of intestinal smooth muscle. Thus, sympathetic fibres, running in the splanchnic outflow, should convey centrally induced inhibitory effects. Exactly how this inhibitory influence is brought about in reflex excitations of the sympatho-adrenal system is, however, not known in detail. At least four principally different modes of action may be considered: (1) Specific, inhibitory sympathetic fibres in direct contact with the intestinal smooth muscles, according to the classical conception. (2) A local ‘overflow’ of the adrenergic transmitter, released at the intestinal vasoconstrictor nerve endings. (3) Local chemical changes induced by the neurogenic reduction of the blood flow to the intestine. (4) Hormones from the suprarenal medulla, released by splanchnic nerve activation.