title: Electrophysiological basis of arteriolar vasomotion in vivo.
abstract: We tested the hypothesis that cyclic changes in membrane potential (E(m)) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (approximately 3 min(-1)) were preceded (approximately 3 s) by oscillations in E(m) of smooth muscle cells (SMC) and endothelial cells (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 diameter observed during vasomotion (41 +/- 2 microm); (2) a slow depolarization (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 transient partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarization (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) at the smallest diameter (27 +/- 2 microm) during vasomotion; (6) a slow repolarization (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 nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO(2) caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E(m) of SMC and EC corresponding with cation fluxes across plasma membranes.
authors.affiliation: John B. Pierce Laboratory, Yale University School of Medicine, New Haven, CT 06519-1403, USA.
authors.forename: I S
authors.initials: IS
authors.lastname: Bartlett
authors.forename: G J
authors.initials: GJ
authors.lastname: Crane
authors.forename: T O
authors.initials: TO
authors.lastname: Neild
authors.forename: S S
authors.initials: SS
authors.lastname: Segal
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001160:Arterioles / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects; D006224:Cricetinae; D004594:Electrophysiology; D007211:Indoles / Q000494:pharmacology; D017136:Ion Transport / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008647:Mesocricetus; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology; D010313:Partial Pressure; D026902:Potassium Channel Blockers; D019789:Tetraethylammonium / Q000494:pharmacology; D014661:Vasoconstriction / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D007211:Indoles; D026902:Potassium Channel Blockers; D014665:Vasodilator Agents; D009599:Nitroprusside; D019789:Tetraethylammonium; D009543:Nifedipine; D010100:Oxygen; D002118:Calcium; C000543:cyclopiazonic acid