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 (∼3 min^–1) were preceded (∼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 µm); (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 µm) 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 PO₂ 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.

Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells

“…It is worth mentioning that accumulating evidence indicate that SR Ca 2+ ATPase functioning/location within the cell (which greatly influences the velocity of calcium upload) determines the mode of Ca 2+ transient in VSMCs. Consistent with this, i) "phasic" VSMCs display a greater number of peripherally located SR than "tonic" VSMCs; indeed "tonic" VSMCs exhibit centrally located SR; (rev in [61,77]); ii) drugs which interfere with the IP3 pathway or intracellular stores abolish spontaneous vasomotion [11,78]; iii) blocking SERCA strongly inhibits the Ca 2+ oscillations, demonstrating that they are induced by SR Ca 2+ release; this latter argument is further supported by the fact that oscillations are present even in the absence of extracellular Ca 2+ [43,45,55,56]. The color intensity reflects Ca 2+ concentrations.…”

Jejunal tissue oxygenation and microvascular flow motion during hemorrhage and resuscitation

“…It has been shown that voltage-operated L-type Ca 2ϩ channels, cGMP, the Na ϩ /K ϩ pump, and the sarcoplasmatic reticulum are part of a biological oscillator system forming the basis for arteriolar vasomotion (1,10,11). Electromechanical coupling with oscillations of smooth muscle cell membrane potential, intracellular Ca 2ϩ , and arteriolar diameter has been demonstrated during hyperoxia in the hamster cheek pouch preparation in vivo (29).…”

Monitoring of rhythms in laser speckle data

“…10,11 The underlying mechanism is based on ionic mechanisms in vascular smooth muscle cells. 12,13 Additional experimental veri¯cation of predictions made on temporal and spatial features of such self-sustained behavior of arterial wall is needed.…”