title: Response of aorta connective tissue matrix to injury caused by vassopressin-induced hypertension or hypercholesterolemia.
abstract: The aim of the study was to investigate the effect of two various atherogenic stimuli (vasopressin-induced hypertension or hypercholesterolemia) on the collagen and glycosaminoglycan (GAG) content in the internal or external part of both thoracic and abdominal aorta, which are differently susceptible to atherosclerosis. Experimental rabbits were divided into four groups: controls, animals injected with physiological saline or vasopressin at the dose of 1 IU/kg from the 1 st to the 25 th day of experiment, respectively. The animals from group 4 were maintained on food, containing 0.25% cholesterol. Only in the vasopressin-treated group, the systolic blood pressure was elevated from 110 mmHg at the beginning, to 166 mmHg at the end of the study. After 14 weeks the aorta was dissected into internal and external parts. GAG fractions were separated and estimated as uronic acids. Collagen was evaluated as the hydroxyproline content in the tissue. Augmented total GAG and heparan sulphate (HS) level, plus no changes in the collagen content were seen in the internal part of the thoracic aorta in rabbits with hypercholesterolemia or hypertension. In the hypertensive animals, the changes were extended to the external part of the aorta and, additionally, comprised the elevation of the chondroitin-4 sulphate (C-4S) content. The two atherogenic stimuli increased the collagen level with no elevation of the GAG content in the abdominal aorta. A convergent effect of the injury, caused by hypertension or hypercholesterolemia on the collagen, total GAG and HS content was shown in the respective parts of the rabbit aortas. The common GAG, increased in the thoracic aorta, stand for the HS, in both hypertensive and hypercholesterolemic rabbits. As the sensitivity to atherosclerosis development in different segments of the aorta varies, they express various responses of the connective tissue matrix to injuries, caused by hypertension or hypercholesterolemia.
authors.affiliation: Department of Pathophysiology, Medical University of Lódz, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Drobnik
authors.forename: R
authors.initials: R
authors.lastname: Dabrowski
authors.forename: A
authors.initials: A
authors.lastname: Szczepanowska
authors.forename: L
authors.initials: L
authors.lastname: Giernat
authors.forename: J
authors.initials: J
authors.lastname: Lorenc
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism*; D001013:Aorta, Thoracic / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood*; D003094:Collagen / Q000378:metabolism*; D003238:Connective Tissue / Q000378:metabolism; D006025:Glycosaminoglycans / Q000378:metabolism*; D006937:Hypercholesterolemia / Q000139:chemically induced / Q000378:metabolism*; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D011817:Rabbits; D014662:Vasoconstrictor Agents; D014667:Vasopressins
chemical_list: D006025:Glycosaminoglycans; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D003094:Collagen; D002784:Cholesterol