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G C Rodrigo

Publications and source records attributed to G C Rodrigo.

21 records · Page 2Linked to original sources

The dependence of the strength of sodium-depletion contractures of isolated frog atrial trabeculae on the membrane potential.

When the Na bathing isolated frog atrial trabeculae voltage clamped at -80 mV is reduced, a strong contracture develops. Upon return to normal extracellular Na concentration [( Na]o) this contracture rapidly relaxes. Hyperpolarization of the membrane by a voltage-clamp pulse during the low-Na contracture produces a rapid relaxation and the extent of this relaxation is dependent upon the size of the hyperpolarizing pulse. The membrane potential at which tension is relaxed to a constant level during low-Na perfusion, is exponentially related to the change in the Na gradient. This relationship shows that changes in the Na gradient, across the cell membrane, have nearly three times more effect on the generation of tension than changes in membrane potential. This would be consistent with the notion that contracture tension is determined by an electrogenic Na/Ca exchange across the cell membrane with a coupling ratio approaching 3 Na+/Ca2+. Exposure of the muscle to strophanthidin reduces the size of the hyperpolarizing pulse required to relax completely the low-Na contracture. As a consequence the apparent coupling ratio is increased to just above 3 Na+/Ca2+. Upon repolarization to -80 mV in low-Na Ringer solution, the redeveloped tension may be larger than that recorded immediately before the hyperpolarizing pulse. This after-effect suggests that hyperpolarization of the membrane may reduce the fall in intracellular [Na] that normally occurs when the bathing [Na] is reduced.

Animals↗

The dependence of the relaxation of tension of frog atrial-trabeculae on the sodium-calcium exchange: a voltage-clamp study.

The dependence of the relaxation of tension of isolated frog atrial trabeculae, upon membrane potential, [Na]0 and [Ca]0, has been studied under voltage-clamp conditions. The change in tension following the repolarization of the membrane potential can be resolved into two phases: an initial phase which opposes relaxation and has an exponential time constant of about 80 ms and is unaffected by changes in either membrane potential, [Na]o or [Ca]o; and a subsequent exponential fall in tension, the rate of which is slowed by depolarization, raised [Ca]o or lowered [Na]o. The dependence of the second phase of relaxation upon the membrane potential is consistent with Ca2+ being removed from the sarcoplasm by an Na-Ca exchange in the cell membrane which has a coupling ratio close to 3 Na+ for each Ca2+. To explain the full effects of changes in [Na]o and [Ca]o upon relaxation with the same Na-Ca exchange stoicheiometry it is necessary to assume that these changes in the bathing fluid affect [Na]i and that relaxation is dependent upon a single unbinding step, involving Ca2+ and the regulatory proteins.

Animals↗

Calcium paradox of the heart: a role for intracellular sodium ions.

Hearts that have been perfused in low calcium fluids suffer, on return to normal calcium solutions, an impairment of function which can be irreversible-- the "calcium paradox." In hypothermic mammalian, amphibian, and fish heart the strong contracture, which is a typical first stage in the development of the calcium paradox, is reversible and appears to depend on a large rise in intracellular Na concentration ([Na]i), which occurs during the period of Ca deprivation. This rise is mainly due to a maintained inward Na flux through the Ca channels and causes a depolarization of the membrane potential, which stabilizes at about -20 mV. In frog atrial muscle if the membrane potential is clamped to values more negative than -50 mV during the period of Ca deprivation, no contracture develops on the restoration of the extracellular Ca concentration ([Ca]o). In all tissues the depolarization, the rise in [Na]i, and the Ca addition contracture are blocked by Ca channel blockers, antiarrhythmic drugs, and Mg ions if present in the Ca-free fluid. These agents are ineffective, however, if applied after a period of Ca deprivation when [Na]i has already risen. The influx of Ca ions, on Ca repletion, is therefore unlikely to be via the Ca channels and would seem to be through the Na-Ca exchange.

Animals↗