title: Carotid sinus baroreceptor reflex control of venular pressure-diameter relations in rat intestine.
abstract: We tested the hypothesis that the venules of the small intestinal muscle are responsible for decreases in vascular capacitance during bilateral carotid artery occlusion. We measured microvascular venular pressure and diameter relations in 135 vessels during both control and baroreflexive conditions (bilateral carotid occlusion). Microvascular pressure was measured using a servo-null pressure system, and diameters were obtained from a video-monitoring system with a total magnification of X1,000. First-, second-, and fourth-order microvenules were studied in rat small intestinal muscle. The vessels showed an average diameter decrease of 11-12% and an increased stiffness or pressure-diameter slope of 31-53% during bilateral occlusion. We also tested whether the observed constriction during bilateral occlusion was caused by an increase in the sympathetic nerve activity to the venules and/or increased hormonal release via the baroreflex system. We studied an additional 22 microvenules before and after denervation of the preparation. Denervation eliminated any significant change in diameter or stiffness during bilateral occlusion. Based on our data, we conclude that the changes in the venular properties observed during bilateral occlusion are due to the increased sympathetic nerve activity resulting from decreased carotid sinus pressure. Intestinal venules can actively constrict to change vascular capacitance during bilateral carotid occlusion.
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
authors.forename: E B
authors.initials: EB
authors.lastname: Haase
authors.forename: A A
authors.initials: AA
authors.lastname: Shoukas
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002346:Carotid Sinus / Q000502:physiology*; D003714:Denervation; D007421:Intestine, Small / Q000098:blood supply; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex / Q000502:physiology*; D014661:Vasoconstriction; D014664:Vasodilation; D014699:Venules / Q000294:innervation / Q000502:physiology*