title: Arterial responses to compromised blood flow.
abstract: Chronic decreases in arterial blood flow rates elicit arterial constriction followed by remodeling of the artery wall that entrenches a reduced internal diameter. This adaptive response may provide an important compensatory adaptation to physiological reductions in blood flow, but it may also exacerbate pathologic disorders that compromise tissue perfusion. A capacity to manipulate this response requires a knowledge of the mechanisms that control it. Our studies have shown that the response is endothelium-dependent, and that it is probably initiated by release of a vasoconstrictor. This finding suggests that endothelium-derived agonist(s) are involved. We assessed the potential role of prostanoids, endothelin, and a local vessel wall renin-angiotensin system. All of these assessments yielded negative results. It appears, therefore, that a novel vasoactive substance initiates the adaptive response of arteries to reduced blood flow.
authors.affiliation: Department of Pathology, University of Toronto, Ontario, Canada.
authors.forename: B L
authors.initials: BL
authors.lastname: Langille
authors.forename: M P
authors.initials: MP
authors.lastname: Bendeck
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D001783:Blood Flow Velocity / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology; D016232:Endothelins / Q000502:physiology; D011453:Prostaglandins / Q000096:biosynthesis; D011817:Rabbits; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012504:Saralasin / Q000494:pharmacology; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D016232:Endothelins; D011453:Prostaglandins; D002216:Captopril; D012504:Saralasin