Electrophysiological basis of arteriolar vasomotion in vivo

Citation
Is. Bartlett et al., Electrophysiological basis of arteriolar vasomotion in vivo, J VASC RES, 37(6), 2000, pp. 568-575
Citations number
27
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF VASCULAR RESEARCH
ISSN journal
10181172 → ACNP
Volume
37
Issue
6
Year of publication
2000
Pages
568 - 575
Database
ISI
SICI code
1018-1172(200011/12)37:6<568:EBOAVI>2.0.ZU;2-3
Abstract
We tested the hypothesis that cyclic changes in membrane potential (E-m) un derlie spontaneous vasomotion in cheek pouch arterioles of anesthetized ham sters, Diameter oscillations (similar to3 min(-1)) were preceded (similar t o3 s) by oscillations in E-m of smooth muscle cells (SMC) and endothelial c ells (EC). Oscillations in E-m were resolved into six phases: (1) a period (6 +/- 2 s) at the most negative E-m observed during vasomotion (-46 +/- 2 mV) correlating (r = 0.87, p < 0.01) with time (8 +/- 2 s) at the largest d iameter observed during vasomotion (41 +/- 2 <mu>m); (2) a slow depolarizat ion (1.8 +/- 0.2 mV s(-1)) with no diameter change; (3) a fast (9.1 +/- 0.8 mV s(-1)) depolarization (to -28 +/- 2 mV) and constriction; (4) a transie nt partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarizat ion (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) a t the smallest diameter (27 +/- 2 <mu>m) during vasomotion; (6) a slow repo larization (2.5 +/- 0.2 mV s(-1)) and relaxation. The absolute change in E- m correlated (r = 0.60, p < 0.01) with the most negative E-m. Sodium nitrop russide or nifedipine caused sustained hyperpolarization and dilation, wher eas tetraethylammonium or elevated PO2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cycl ic changes in E-m of SMC and EC corresponding with cation fluxes across pla sma membranes. Copyright (C) 2000 S. Karger AG, Basel.