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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied relaxation during rapid rewarming of rabbit ventricular muscles that had been activated by rapid cooling. Rewarming from 1 degree to 30 degrees C (in less than 0.5 second) activates mechanisms that contribute to the reduction of intracellular calcium concentration and thus relaxation (e.g., sarcoplasmic reticulum [SR] calcium pump and sarcolemmal Na-Ca exchange and calcium pump). Rapid rewarming in normal Tyrode's solution induces relaxation with a half-time (t1/2) of 217 +/- 14 msec (mean +/- SEM). During cold exposure, changing the superfusate to a sodium-free, calcium-free medium with 2 mM CoCl2 (to eliminate Na-Ca exchange) slightly slows relaxation upon rewarming in the same medium (t1/2 = 279 +/- 44 msec). Addition of 10 mM caffeine (which prevents SR calcium sequestration) to normal Tyrode's solution during cold superfusion slows relaxation somewhat more (t1/2 = 376 +/- 31 msec) than sodium-free, calcium-free solution. However, if both interventions are combined (sodium-free + caffeine) during the cold exposure and rewarming, the relaxation is greatly slowed (t1/2 = 2,580 +/- 810 msec). These results suggest that either the SR calcium pump or, to a lesser extent, sarcolemmal Na-Ca exchange can produce rapid relaxation, but if both systems are blocked, relaxation is very slow. If muscles are equilibrated with 500 nM ryanodine before cooling, relaxation upon rewarming is not greatly slowed (t1/2 = 266 +/- 37 msec) even if sodium-free, calcium-free solution is applied during the cold and rewarming phases (t1/2 = 305 +/- 66 msec). This result suggests that ryanodine does not prevent the SR from accumulating calcium to induce relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity. 254 95

Normally the sarcoplasmic reticular calcium pump and sarcolemmal Na/Ca exchange compete and are the primary mechanisms responsible for reducing [Ca]i during cardiac relaxation. The sarcolemmal calcium pump and mitochondrial calcium uptake are much slower, but may also participate in [Ca]i regulation. The aim of this study was to provide a clearer understanding of the interaction of these mechanisms. Myocyte shortening and [Ca]i transients (using indo-1 fluorescence) were measured in rabbit ventricular myocytes, with similar results. The t1/2 of twitch relaxation was 0.17(SEM 0.03) s. Contractures induced by 10 mM caffeine (caffeine contraction) relaxed more slowly [t1/2 = 0.54(0.07) s] due to prevention of sarcoplasmic reticular calcium uptake. When the Na/Ca exchange was also blocked by perfusion with 0Na,0Ca solution, the peak of the caffeine contraction was increased (by 44%) and relaxation was slowed about 16-fold [t1/2 = 8.8(0.8) s]. Blocking mitochondrial calcium uptake by including 1 microM FCCP + 1 microM oligomycin in the 0Na,0Ca solution slowed the relaxation of the caffeine contraction further [t1/2 = 19.7(3.2) s]. Inhibition of the sarcolemmal calcium pump by perfusion with 0Na, 10 mM Ca during caffeine contraction also increased the relaxation t1/2 to 27.5(6.9) s. Inhibition of all four calcium transport systems almost abolished relaxation. It is also shown that calcium which was taken up by the mitochondria during relaxation of the caffeine contraction in 0Na,0Ca gradually redistributed (with tau = 41 s) back to the sarcoplasmic reticulum after caffeine was removed. A second caffeine contraction could then be elicited.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Competition and redistribution among calcium transport systems in rabbit cardiac myocytes. 827 22

Although evidence suggests that high intracellular calcium activity ([Ca2+]i) inhibits sperm motility, data concerning [Ca2+]i within, or slightly above, the physiological range are sparse, particularly in mammalian sperm. We investigated inhibitors of the sarcoplasmic/endoplasmic reticulum Ca-ATPase (SERCA) and the plasma membrane Ca-ATPase with the objective of increasing the intracellular calcium ion activity in human spermatozoa to study its effect on motility and other functions. Thapsigargin (20 micromol/L) increased [Ca2+]i from 140 +/- 7 nmol/L over an approximately 2-min period to reach a plateau of 530 +/- 84 nmol/L (mean +/- SEM, n = 3, p < 0.05). In sperm suspended in calcium-free medium thapsigargin increased [Ca2+]i from 13 +/- 3.3 to 35 +/- 7.5 nmol/L (p < 0.01), consistent with the release of calcium from intracellular stores. Cyclopiazonic acid (60 micromol/L) caused a transient decrease in [Ca2+]i. Quercetin, (200 micromol/L) caused a rapid increase in [Ca2+]i to 1280 +/- 90 nmol/L, after which [Ca2+]i fell quickly at first but then more slowly. Thapsigargin (20 micromol/L) caused approximately 70% of sperm to acrosome react in < or = 5 min, but once acrosome reacted, many sperm died over the next 30 min. Lower concentrations of thapsigargin caused fewer acrosome reactions but were less toxic. Both thapsigargin and quercetin caused rapid dose-dependent decreases in sperm motility. The results are consistent with high [Ca2+]i in the range observed in caput epididymal or cryopreserved spermatozoa inhibiting motility, but might be confounded by other events following the acrosome reaction.
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PMID:Effects of Ca-ATPase inhibitors on the intracellular calcium activity and motility of human spermatozoa. 1463 22