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Vol. 288, Issue 3, 1037-1044, March 1999
Pharmacie Clinique, Faculté de Pharmacie (F.B., R.F.),
Chatenay Malabry, France;
Institut National de la Santé et de la
Recherche Médicale (INSERM) U410, Faculté de Médecine
X Bichat (F.B., S.J., A.T., J.C., C.R.), Paris, France; and
INSERM U13,
CHU Bichat Claude Bernard (C.C.), Paris, France
Intestinal absorption of 
-lactamine antibiotics (e.g.,
cefixime and cephalexin) has been shown to proceed through the
dipeptide carrier system. In a previous study, nifedipine (NFP), an
L-type calcium channel blocker, enhanced the absorption of cefixime in vivo but not in vitro, and it was suggested that neural mechanisms might be involved in the effect of NFP. The aim of the present study
was to assess the involvement of the nervous system on the intestinal
absorption of cephalexin (CFX). To investigate this, we used a
single-pass jejunal perfusion technique in rats. NFP and diltiazem
enhanced approximately 2-fold the plasma levels of CFX in treated
rats versus untreated controls. NFP also increased approximately
2-fold the CFX level in portal plasma and increased urinary excretion
of CFX, thus indicating that CFX did effectively increase CFX
intestinal absorption. Perfusing high concentrations of dipeptides in
the jejunal lumen competitively reduced CFX absorption and inhibited
the enhancement of CFX absorption produced by NFP. Hexamethonium and
lidocaine inhibited the effect of NFP, whereas atropine, capsaicin,
clonidine, and isoproterenol enhanced CFX absorption by the same order
of magnitude as NFP. Thus, complex neural networks can modulate the
function of the intestinal di- and tripeptide transporter. Sympathetic
noradrenergic fibers, intestinal sensory neurons, and nicotinic
synapses are involved in the increase of CFX absorption produced by NFP.
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