Electrical and mechanical responses of rat saphenous vein to short-term pressure load. Am J Physiol 1989 Jan;256(1 Pt 2):H47-55
Date
01/11/1989Pubmed ID
2912197DOI
10.1152/ajpheart.1989.256.1.H47Scopus ID
2-s2.0-0024545236 (requires institutional sign-in at Scopus site) 25 CitationsAbstract
The magnitude and mechanism of myogenic response of vascular smooth muscle (SM) in rat distal saphenous vein was assessed from SM membrane potential (Em) measured in situ and in vitro with glass microelectrodes and from active and passive stress and strain calculated from changes in vessel diameter measured in vitro via videomicroscopy. Elevation of intraluminal pressure from 2.2 +/- 0.2 (SE) mmHg (control) to 15 +/- 0.8 mmHg for 1 h in a series of in vitro vessel segments perfused with physiological salt solution at 0.2 ml/min induced a maintained and reversible depolarization of 18 +/- 0.9 mV. A 7.6 +/- 0.4-mmHg pressure increase induced a 12.9 +/- 1.2-mV depolarization in a second series. In a third series, 5-mmHg pressure increments induced significant increments in active isometric stress and isobaric strain. Opening an acute, reversible in situ femoral artery to saphenous vein shunt caused a 4- to 5-mmHg venous pressure elevation, a 10-fold increase in venous blood flow, and a 12.1 +/- 0.9-mV venous SM depolarization. Thus a short-term pressure load causes sustained, reversible venous SM cell depolarization both in vitro and in situ, coupled with active strain and stress generation in the vein wall. These results support our hypothesis that SM of peripheral veins can contribute to an intrinsic capacity autoregulation.
Author List
Monos E, Contney SJ, Cowley AW Jr, Stekiel WJAuthor
Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AlgorithmsAnimals
Electrophysiology
Homeostasis
Male
Membrane Potentials
Microelectrodes
Muscle, Smooth, Vascular
Pressure
Rats
Rats, Inbred Strains
Saphenous Vein
