Quantum-fluctuation-induced repelling interaction of quantum string between walls

Quantum string, which was brought into discussion recently as a model for the stripe phase in doped cuprates, is simulated by means of the density-matrix-renormalization-group method. String collides with adjacent neighbors, as it wonders, owing to quantum zero-point fluctuations. The energy cost due to the collisions is our main concern. Embedding a quantum string between rigid walls with separation d, we found that for sufficiently large d, collision-induced energy cost obeys the formula \sim exp (- A d^alpha) with alpha=0.808(1), and string's mean fluctuation width grows logarithmically \sim log d. Those results are not understood in terms of conventional picture that the string is `disordered,' and only the short-wave-length fluctuations contribute to collisions. Rather, our results support a recent proposal that owing to collisions, short-wave-length fluctuations are suppressed, but instead, long-wave-length fluctuations become significant. This mechanism would be responsible for stabilizing the stripe phase

Involvement of K channels and calcium-independent mechanisms in hydrogen sulfide-induced relaxation of rat mesenteric small arteries.

Endogenous hydrogen sulfide (H2S) is involved in the regulation of vascular tone. We hypothesized that lowering of calcium and opening of K channels as well as calcium-independent mechanisms are involved in H2S-induced relaxation in rat mesenteric small arteries. Amperometric recordings revealed that free [H2S] after addition to closed tubes of NaSH, Na2S, and GYY4137 were, respectively, 14%, 17%, and 1% of added amount. The compounds caused equipotent relaxations in isometric myographs, but based on the measured free [H2S], GYY4137 caused more relaxation in relation to released free [H2S] than NaSH and Na2S in rat mesenteric small arteries. Simultaneous measurements of [H2S] and tension showed that 15 μM of free H2S caused 61% relaxation in superior mesenteric arteries. Simultaneous measurements of smooth muscle calcium and tension revealed that NaSH lowered calcium and caused relaxation of norepinephrine-contracted arteries, while high extracellular potassium reduced NaSH relaxation without corresponding calcium changes. In norepinephrine-contracted arteries, NaSH (1 mM) lowered phosphorylation of myosin light chain, while phosphorylation of myosin phosphatase target subunit 1 (MYPT-1) remained unchanged. Inhibitors of guanylate cyclase, protein kinase A and G failed to reduce NaSH relaxation, while blockers of voltage-gated KV7 channels inhibited NaSH relaxation, and blockers of mitochondrial complex I and III abolished NaSH relaxation. CONCLUSION: the present findings suggest that low micromolar concentrations of free H2S by a dual mechanism opens K channels followed by lowering of smooth muscle calcium and by a mechanism involving mitochondrial complex I and III leads to uncoupling of force, and hence vasodilation