The effects of changes of pH on intracellular calcium transients in mammalian cardiac muscle.

Abstract

monophasic decline in developed tension, and a small increase in peak light. Alkaloses produced by changing the [HC03-]/[C02] ratio produced similarresults but the changes observed were in the opposite direction to those described above.6. The effects of changes of pHo can be explained if pHi affects tension by two mechanisms. The first mechanism, which is responsible for the rapid change in tension, is not associated with a change in [Ca2+]j. The second mechanism leads to a slower and smaller change in tension, in the opposite direction to the first, and is due to a change in the intracellular calcium transient.

Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats

“…Systolic cytosolic calcium concentration ([Ca2+]i) is usually far from saturating the contractile proteins (Fabiato, 1981) (Allen & Orchard, 1983). It is, therefore, possible that the increased or decreased sensitivities to verapamil or nifedipine during hyperventilation or hypoventilation, respectively, as observed in the present study, may be due to up-or downregulation of one or more of these steps leading to cellular contraction.…”

Acidosis in models of cardiac ventricular myocytes

“…This decrease is faster in response to interventions that rapidly alter intracellular, rather than extracellular, pH, indicating that intracellular acidosis is responsible for the decrease (Vaughan-Jones et al 1987). During prolonged exposure to acidosis a secondary recovery of developed force can also be observed (Allen & Orchard 1983;Orchard 1987).…”

“…The time course of the transient is prolonged (Allen & Orchard 1983;Orchard 1987). Thus, it appears that the decrease in developed force is not due to a decrease of activating Ca 2C , and it is now generally accepted that the negative inotropic effect of acidosis is due predominantly to a decrease in the sensitivity of the contractile proteins to Ca 2C (Fabiato & Fabiato 1978;Solaro et al 1989;Orchard & Kentish 1990).…”

“…Thus, it appears that the decrease in developed force is not due to a decrease of activating Ca 2C , and it is now generally accepted that the negative inotropic effect of acidosis is due predominantly to a decrease in the sensitivity of the contractile proteins to Ca 2C (Fabiato & Fabiato 1978;Solaro et al 1989;Orchard & Kentish 1990). The secondary recovery of developed force that occurs during acidosis is, however, accompanied by (i) an increase in diastolic Ca 2C , (ii) an increase in the amplitude of the systolic Ca 2C transient, which appears to underlie the contractile recovery and (iii) recovery of the time course of the Ca 2C transient (Allen & Orchard 1983;Orchard 1987;Harrison et al 1992;DeSantiago et al 2004).…”

Na + /H + Exchange Inhibition With HOE642 Improves Postischemic Recovery due to Attenuation of Ca 2+ Overload and Prolonged Acidosis on Reperfusion

“…29 However, because pH i was comparable in both groups during ischemia and during the first minute of reperfusion, [Ca 2ϩ ] i values quantified with the use of fractional luminescence were underestimated, but the relative differences between the treated and untreated hearts were unaffected.…”