title: Short-Term biomechanical adaptation of the rat carotid to acute hypertension: contribution of smooth muscle.
abstract: The biomechanical adaptation of the arterial wall to hypertension has been studied extensively in recent years; however, the exact biomechanical contribution of vascular smooth muscle cells (VSMCs) during the adaptation process in conduit vessels is not known. We induced hypertension in 8 wk old Wistar rats by total ligation of the aorta between the two kidneys. Mean blood pressure increased from 92 +/- 2 (mean +/- SE) mm Hg to approximately 150 mmHg. Rats were sacrificed 2, 4, and 8 d after surgery and the left common carotid artery was excised for analysis. Wall thickness increased by 18% in 8 d and the opening angle by 32% in 4 d. The elastic properties were measured under normal VSMC tone (i.e., the amount of VSMC tone under normal conditions also called basal VSMC tone or normal resting VSMC tone), under maximally contracted VSMC (NE, 5 x 10(-7) mol/L) and under totally relaxed VSMC conditions (papaverine, 10(-4) mol/L). The most pronounced modifications were the changes in elastic properties related to normal VSMC tone. The functional contraction ratio at 100 mm Hg, defined as the relative contraction under normal conditions (normal VSMC tone), increased by 439% 4 d after the induction of hypertension. The total contraction capacity of the VSMC increased by 38% within 8 d. The changes in normal VSMC tone led to important changes in the mechanical properties of the arterial wall. Under normal VSMC conditions, compliance at mean pressure (148 mm Hg) increased by 159% within 8 d, whereas in the absence of VSMC tone, compliance did not increase significantly. We conclude that in conduit vessels, the VSMC, which is the sensing and effecting element of the adaptation process, is subjected to large-scale changes during the early phase of arterial adaptation to acute hypertension.
authors.affiliation: Biomedical Engineering Laboratory, Swiss Federal Institute of Technology, Lausanne.
authors.forename: P
authors.initials: P
authors.lastname: Fridez
authors.forename: A
authors.initials: A
authors.lastname: Makino
authors.forename: H
authors.initials: H
authors.lastname: Miyazaki
authors.forename: J J
authors.initials: JJ
authors.lastname: Meister
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
authors.forename: N
authors.initials: N
authors.lastname: Stergiopulos
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001012:Aorta, Abdominal / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000503:physiopathology; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D017536:Carotid Artery, Common / Q000503:physiopathology; D004548:Elasticity; D006973:Hypertension / Q000503:physiopathology*; D008026:Ligation; D009129:Muscle Tonus; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical