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[Mechanism of nitric oxide's effect on the sensitivity of smooth muscle contractions to calcium].

It was investigated whether the SH-groups of contractile proteins are involved in NO-induced relaxation of saponin-skinned smooth muscle strips. Both, the thiol-specific alkylating agent N-ethylmaleamide (NEM), and thiol-reducing agent dithiotreitol (DTT) induced relaxation of maximally activated skinned rat portal vein preparations. The relaxing effects of DTT and nitric oxide donor sodium nitroprusside were not additive. After the relaxation, induced by one of this agent, the effect of the other one was negligible. We suggest that NO-induced smooth muscle relaxation be due to decreasing of force sensitivity to Ca2+. This effect of nitric oxide is realized by its interaction with critical thiol groups of smooth muscle contractile proteins.

Animals↗

Muscle contraction during hyperpolarizing currents in the crab.

Isolated muscle fibers from the motor legs of the crab Trichodactilus dilocarcinus were submitted to strong hyperpolarizing currents of varied intensities which produced tension during the current pulse. Threshold for tension was obtained with intensities of about 0.2 x 10(-5) A, changing E(m) to ca. -150 mV (starting from a resting potential ofca. -80 mV). At the closure of the anodic square pulse, a second phase of tension usually appeared superimposed upon the one obtained during hyperpolarization. The first phase of tension increased with the increase of Ca(++) concentration in the bath. Sr(++) produced the same type of mechanical output as Ca(++). When added to the normal Ca(++) concentration, Ba(++) and Mn(++) in low concentrations (up to 21.5 mM) also increased the tension of this phase, but at higher concentrations they blocked both phases while Mg(++) did not alter the tension. Of all the divalent cations employed, only Sr(++) is capable of developing tension as a substitute for Ca(++) in the external media. Procaine administered in a dosage (5 x 10(-3) W/V)which would suppress the contracture due to caffeine (10 mM), did not modify the tension developed during the hyperpolarization. The preceding data indicate that the Ca(++) required for tension during hyperpolarization comes from sites which would differ from those usually postulated for tension due to depolarization in the muscle fibers of other crustaceans (American crayfish). Furthermore, the external source of Ca(++) appears to be one mainly implicated in the induction of tension due to inward current pulses.

Animals↗