AHEART September 46/
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چکیده
Segal, Steven S., Suzanne E. Brett, and William C. Sessa. Codistribution of NOS and caveolin throughout peripheral vasculature and skeletal muscle of hamsters. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1167–H1177, 1999.—In isolated cell systems, nitric oxide synthase (NOS) activity is regulated by caveolin (CAV), a resident caveolae coat protein. Because little is known of this interaction in vivo, we tested whether NOS and caveolin are distributed together in the intact organism. Using immunohistochemistry, we investigated the localization of constitutive neuronal (nNOS) and endothelial (eNOS) enzyme isoforms along with caveolin-1 (CAV-1) and caveolin-3 (CAV-3) throughout the systemic vasculature and peripheral tissues of the hamster. The carotid artery, abdominal aorta, vena cava, femoral artery and vein, feed artery and collecting vein of the cheek pouch retractor muscle, capillaries and muscle fibers of retractor and cremaster muscles, and arterioles and venules of the cheek pouch were studied. In endothelial cells, eNOS and CAV-1 were present throughout the vasculature, whereas nNOS and CAV-3 were absent except in capillaries, which reacted for nNOS. In smooth muscle cells, nNOS and CAV-1 were also expressed systemically, whereas eNOS was absent; CAV-3 was present in the arterial but not the venous vasculature. Both nNOS and CAV-3 were located at the sarcolemma of skeletal muscle fibers, which were devoid of eNOS and CAV-1. These immunolabeling patterns suggest functional interactions between eNOS and CAV-1 throughout the endothelium, regional differences in the modulation of nNOS by caveolin isoforms in vascular smooth muscle, and modulation of nNOS by CAV-3 in skeletal muscle.
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AHEART September 46/
DOUGLAS R. SEALS, EDITH T. STEVENSON, PAMELA P. JONES, CHRISTOPHER A. DESOUZA, AND HIROFUMI TANAKA (With the Technical Assistance of Cyndi Long and Mary Jo Reiling) Human Cardiovascular Research Laboratory, Center for Physical Activity, Disease Prevention, and Aging, Department of Kinesiology and Applied Physiology, University of Colorado, Boulder 80309, and Department of Medicine, Divisions of...
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FERENC DOMOKI,1,3 ROLAND VELTKAMP,1,2 NISHADI THRIKAWALA,1 GREG ROBINS,1 FERENC BARI,1,3 THOMAS M. LOUIS,4 AND DAVID W. BUSIJA1 1Department of Physiology and Pharmacology and 2Stroke Research Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1083; 3Department of Physiology, Albert Szent-Györgyi Medical University, Szeged, H-6720 Hungary; 4Department of Anato...
متن کاملAHEART September 46/
Gyenge, C. C., B. D. Bowen, R. K. Reed, and J. L. Bert. Transport of fluid and solutes in the body. I. Formulation of a mathematical model. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1215–H1227, 1999.—A compartmental model of shortterm whole body fluid, protein, and ion distribution and transport is formulated. The model comprises four compartments: a vascular and an interstitial compartme...
متن کاملAHEART October 46/4
F. COCEANI,1 Y.-A. LIU,1 E. SEIDLITZ,1 L. KELSEY,1 T. KUWAKI,3 C. ACKERLEY,2 AND M. YANAGISAWA4 1Integrative Biology Programme and 2Division of Pathology, The Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8; 3Department of Physiology, School of Medicine, Chiba University, Chiba, 260-8670 Japan; and 4Howard Hughes Medical Institute and Department of Molecular Genetics, University of...
متن کاملAHEART November 46/5
RAGAVENDRA R. BALIGA,1 DAVID R. PIMENTAL,1 YOU-YANG ZHAO,2 WILLIAM W. SIMMONS,1 MARK A. MARCHIONNI,3 DOUGLAS B. SAWYER,1 AND RALPH A. KELLY1 1Cardiovascular Division, Brigham and Women’s Hospital and Harvard Medical School, Boston 02115; 3Cambridge Neurosciences, Cambridge, Massachusetts 02139; and 2Department of Medicine, University of California at San Diego School of Medicine, La Jolla, Cali...
متن کاملAHEART September 46/
Parthimos, D., D. H. Edwards, and T. M. Griffith. Minimal model of arterial chaos generated by coupled intracellular and membrane Ca21 oscillators. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1119–H1144, 1999.—We have developed a mathematical model of arterial vasomotion in which irregular rhythmic activity is generated by the nonlinear interaction of intracellular and membrane oscillators ...
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