Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice

Citation
R. Mancinelli et al., Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice, EXP PHYSIOL, 84(5), 1999, pp. 929-940
Citations number
34
Categorie Soggetti
Physiology
Journal title
EXPERIMENTAL PHYSIOLOGY
ISSN journal
09580670 → ACNP
Volume
84
Issue
5
Year of publication
1999
Pages
929 - 940
Database
ISI
SICI code
0958-0670(199909)84:5<929:MPOSMP>2.0.ZU;2-D
Abstract
Mechanical properties of the vascular smooth muscle from normal and dystrop hin-deficient (mdx) mice were examined. Changes in resting and developed te nsions in response to stretch were recorded in isolated portal vein. The va scular segments were elongated in 5% increments of the 'in situ' length (L- r) up to 1.30L(r). The resting length-tension curves in male mdx mice were similar to normal mice, while a marked decrease in the slope of the curve w as noted in female mdx mice. These findings were not affected by atropine, phentolamine, tetrodotoxin or [Ca2+] in the surrounding media. At L-r, the tension of isolated portal vein was characterized by spontaneous synchroniz ed uniform force waves in normal mouse. In contrast, in mdx mouse portal ve ins an irregular motor pattern characterized by desynchronized Force waves with a decrease of amplitude and an increase in frequency was recorded. Ext ension of the length of the portal vein segment did not increase the sponta neous phasic activity developed in female mdx mice although this was noted with male mdx mice and normal mice. Experiments with chemical depolarizing agents indicated that spontaneous myogenic excitation activated the great m ajority of vascular smooth muscle cells in normal mouse portal vein, wherea s in mdx mice only a reduced number of these cells were excited suggesting that in the mdx mouse the intercellular electronic coupling is altered. In conclusion this study provides the first description of the mechanical acti vities of portal vein longitudinal muscle and shows that in mds mice the mo tor activity is severely disrupted.