AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 2 162-G167, Copyright © 1988 by American Physiological Society
Neurohumoral control of villous motility
W. A. Womack, D. Mailman, P. R. Kvietys and D. N. Granger
Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.
A quantitative videomicroscopic method was used to examine neurohumoral
control of villous motility. Intraduodenal instillation of saline, 0.4%
hydrochloric acid, or acidified predigested food did not cause a
significant change in villous contraction frequency in an isolated segment
of jejunum. Villous motility in the jejunum of fed dogs, from which the
chyme had been removed, was not greater than that in fasted dogs (2.9 +/-
0.3 vs. 3.4 +/- 0.5 contractions/min). Furthermore, acid extracts of the
duodenal mucosa did not produce an increase in jejunal villous motility
when injected intravenously. These data argue against the existence of a
humoral stimulant of villous motility (villikinin). Vagotomy caused only a
small (20%) and transient (10 min) decline in villous motility. Vagal
stimulation at 5, 10, and 20 Hz caused villous motility to increase by 24
+/- 7, 23 +/- 9, and 32 +/- 10%, respectively. Atropine blocked the effects
of vagal stimulation. Section of the periarterial (sympathetic) nerves did
not alter villous contractile activity. Stimulation of the periarterial
nerves at 5, 10, and 20 Hz caused villous contraction frequency to decline
by 41 +/- 5, 45 +/- 5, and 38 +/- 10%, respectively. This inhibition
appears to involve both alpha- and beta-adrenergic receptors and a
reduction in blood flow. Neither atropine, alpha-blockade, nor
beta-blockade produced a sustained alteration in basal contraction
frequency.
