title: Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice.
abstract: Mechanical properties of the vascular smooth muscle from normal and dystrophin-deficient (mdx) mice were examined. Changes in resting and developed tensions in response to stretch were recorded in isolated portal vein. The vascular segments were elongated in 5 % increments of the 'in situ' length (Lr) up to 1.30Lr. The resting length-tension curves in male mdxmice were similar to normal mice, while a marked decrease in the slope of the curve was noted in female mdx mice. These findings were not affected by atropine, phentolamine, tetrodotoxin or [Ca2+] in the surrounding media. At Lr, the tension of isolated portal vein was characterized by spontaneous synchronized uniform force waves in normal mouse. In contrast, in mdxmouse portal veins an irregular motor pattern characterized by desynchronized force waves with a decrease of amplitude and an increase in frequency was recorded. Extension of the length of the portal vein segment did not increase the spontaneous 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 majority of vascular smooth muscle cells in normal mouse portal vein, whereas 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 activities of portal vein longitudinal muscle and shows that in mdx mice the motor activity is severely disrupted.
authors.affiliation: Department of Biochemistry and Human Physiology, Section of Physiology and Human Nutrition, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Mancinelli
authors.forename: P
authors.initials: P
authors.lastname: Tonali
authors.forename: R
authors.initials: R
authors.lastname: Romani
authors.forename: A
authors.initials: A
authors.lastname: Tringali
authors.forename: R
authors.initials: R
authors.lastname: Vargiu
authors.forename: G B
authors.initials: GB
authors.lastname: AZZENA
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016189:Dystrophin / Q000172:deficiency*; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D010812:Physical Stimulation; D011169:Portal Vein / Q000187:drug effects / Q000503:physiopathology*; D011189:Potassium Chloride / Q000378:metabolism; D012016:Reference Values; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000503:physiopathology
chemical_list: D016189:Dystrophin; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D011189:Potassium Chloride; D000109:Acetylcholine; D009638:Norepinephrine