Microprocessor-controlled changes of [free Ca2+] at the outer surface of the sarcoplasmic reticulum (SR) wrapped around individual myofibrils of a skinned canine cardiac Purkinje cell and aequorin bioluminescence recording were used to study the mechanism of Ca2+-induced release of Ca2+ from the SR. This Ca2+ release is triggered by a rapid increase of [free Ca2+] at the outer surface of the SR of a previously quiescent skinned cell. Ca2+-induced release of Ca2+ occurred under conditions that prevented any synthesis of ATP from ADP, was affected differentially by interventions that depressed the SR Ca2+ pump about equally, and required ionic conditions incompatible with all known Ca2+-releasing, uncoupled, partial reactions of the Ca2+ pump. Increasing the [free Ca2+]trigger up to an optimum increased the amount of Ca2+ released. A supraoptimum increase of [free Ca2+] trigger inactivated Ca2+-induced release of Ca2+, but partial inactivation was also observed at [free Ca2+] below that necessary for its activation. The amplitude of the Ca2+ release induced by a given increase of [free Ca2+] decreased when the rate of this increase was diminished. These results suggest that Ca2+-induced release of Ca2+ is through a channel across the SR membrane with time- and Ca2+-dependent activation and inactivation. The inactivating binding site would have a higher affinity for Ca2+ but a lower rate constant than the activating site. Inactivation appeared to be a first-order kinetic reaction of Ca2+ binding to a single site at the outer face of the SR with a Q10 of 1.68. The removal of inactivation was the slowest step of the cycle, responsible for a highly temperature-dependent (Q10 approximately 4.00) refractory period.

https://rupress.org/jgp/article-pdf/85/2/247/1248727/247.pdf

Time and calcium dependence of activation and inactivation of calcium-induced release of calcium from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell.

�Microprocessor-controlled changes of [free Ca 2 '] at the outer surface of the Sarcoplasmic reticulum (SR) wrapped around individual myofibrils of a skinned canine cardiac Purkinje cell and aequorin bioluminescence recording were used to study the mechanism of Ca 2 '-induced release of Ca 21 from the SR . This Ca2' release is triggered by a rapid increase of [free Ca 21] at the outersurface of the SR of a previously quiescent skinned cell . Ca 2 '-induced

Calcium-induced Release of Calcium from the Sarcoplasmic Reticulum of a Skinned Canine Cardiac Purkinje Cell

Myocardiopathy is common in uremia, but its cause in unknown. Excessive entry of calcium in heart cells by catecholamines has been shown to cause necrosis of myocardium. The high blood levels of parathyroid hormone (PTH) in uremia may also enhance entry of calcium into heart cells and exert deleterious effects on the heart. We examined the effect of PTH on rat heart cells grown in culture. Both amino-terminal (1-34) PTH and intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH produced immediate and sustained significant rise in beats per minute and the cells died earlier than control. The effect was reversed if PTH was removed from medium, and was abolished by inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the rise in heart beats, but the effect of 1-84 PTH was significantly greater than that of 1-34 moiety. PTH stimulated cyclic AMP production within 1 min, and cyclic AMP remained significantly elevated thereafter. The effect of PTH required calcium, was mimicked by calcium ionophore, was prevented by verapamil and was not abolished by alpha- or beta-adrenergic blockers. PTH action was additive to phenylephrine and synergistic with isoproterenol. Sera from uremic parathyroidectomized rats did not effect heart beats, but sera from uremic rats with intact parathyroid glands or from uremic-parathyroidectomized rats treated with PTH had effects similar to PTH. Data indicate that (a) heart cell is a target organ for PTH and may have receptors for the hormone; (b) PTH increases beating rate of heart cells and causes early death of cells; (c) PTH effect appears to be due to calcium entry into heart cells; (d) the locus of action through which PTH induces calcium entry is different from that for catecholamines; and (e) uremic serum has no effect unless it contains PTH. Data suggest that myocardial damage may occur in uremia due to prolonged exposure to very high blood levels of PTH, and assign new dimensions to PTH toxicity in uremia.

/pdf/effect-of-parathyroid-hormone-on-rat-heart-cells-1g0hed92qs.pdf

Effect of parathyroid hormone on rat heart cells.

Maximal isometric forces during both twitch and tetanus are largely temperature independent in muscles from both endothermic and ectothermic vertebrates. Anuran muscle can develop maximal force at lower temperatures than mammalian muscle. Tetanic tension is maximal at normally experienced body temperatures in a variety of animals, but twitch tension seldom is. Thermal dependence of twitch tension varies with muscle fiber type: tension decreases with increasing temperature in fast-twitch muscles and remains constant in slow-twitch muscles. In contrast to the low temperature dependence of force generation, rates of development of tension (time to peak twitch tension and tetanic rise time) and maximal velocity of shortening and power output are markedly temperature dependent, with average temperature coefficient (Q10) values of 2.0-2.5 Q10 values for rate processes of anuran muscle are only slightly lower than those of mammalian muscle. High body temperatures permit rapid rates of muscle contraction; animals active at low body temperatures do not achieve the maximal rate performance their muscles are capable of delivering. Thermal acclimation or hibernation does not appear to result in compensatory adjustments in either force generation or rate processes. In vivo, dynamic processes dependent on contractile rates are positively temperature dependent, although with markedly lower Q10 values than those of isolated muscle. Static force application in vivo is nearly temperature independent.

Thermal dependence of muscle function

Correlation of the localization of La+++ with its effects on Ca++ exchange in cultured rat heart cells is examined with the use of a recently developed technique. 75% of cellular Ca++ is exchangeable and is completely accounted for by two kinetically defined phases. The rapidly exchangeable phase has a t ½ = 1.15 min and accounts for 1 1 mmoles Ca++/kg wet cells or 43% of the exchangeable Ca++ (cells perfused with [Ca++]o = 1 mM) Phase 2 has a t ½ = 19.2 min and accounts for 1.5 mmoles Ca++/kg wet cells or 57% of the exchangeable Ca++. 0.5 mM [La+++]o displaces 0 52 mmoles Ca++/kg wet cells—all from phase 1—and almost completely abolishes subsequent Ca++ influx and efflux The presence of La+++ in the washout converts the washout pattern to a single phase system with a t ½ = 124 min. The effects upon Ca++ exchange are coincident with abolition of contractile tension but regenerative depolarization of the tissue is maintained Electron microscope localization of the La+++ places it exclusively in the external lamina or basement membrane of the cells. The study indicates that negatively charged sites in the basement membrane play a crucial role in the E-C coupling process in heart muscle

/pdf/lanthanum-in-heart-cell-culture-effect-on-calcium-exchange-47dteov1uq.pdf

LANTHANUM IN HEART CELL CULTURE : Effect on Calcium Exchange Correlated with Its Localization

Arterially cannulated rabbit interventricular septal tissue was exposed to 5–40 µM La in 2.5 mM Ca perfusate. Immediately following perfusion with La two concurrent events were consistently observed: (a) a rapid decline of active tension to a lesser steady-state value, and (b) an abrupt, release of short duration of tissue-bound Ca. The magnitude of both events was directly related to the [La]o. If the duration of exposure to La was brief, contractility returned toward normal upon return to the La-free perfusate. Elevation of [Ca]o during exposure to La counteracted its effect and induced a concurrent displacement of tissue-bound La. Cellular action potentials recorded during brief perfusion with La demonstrated that essentially normal regenerative depolarization was maintained. Analysis of the quantities of 45Ca released following exposure to 10 µM La indicated that this La-susceptible Ca was being displaced from a homogeneous pool—the one previously shown by Langer to represent contractile dependent Ca. These data led to the following conclusions: During perfusion with 2.5 mM Ca contractile dependent Ca was derived primarily from "superficially" located sites. La effected the release of contractile dependent Ca by modifying the normal permselectivity of this "superficial" membrane for activator Ca. These and other data infer that contractile dependent Ca is derived primarily from superficially located sites.

https://rupress.org/jgp/article-pdf/56/2/191/1244895/191.pdf

Specific Uncoupling of Excitation and Contraction in Mammalian Cardiac Tissue by Lanthanum Kinetic studies

The mechanical responses (active and resting tension, dP/dt, TPT) and ionic exchange characteristics (Ca++, K+, Na+) which follow upon a variation in temperature, rate, and [K+]0 were studied in the rabbit papillary muscle and arterially perfused rabbit interventricular setpum. Abrupt changes in temperature provided a means of separating the contributions of rate of development (intensity) of active state and duration of active state to total active tension development (approximated by isometric tension). Threefold changes in duration of active state with proportional changes in active tension can be induced without evidence for alteration of Ca++, K+, or Na+ exchange. Abrupt cooling produced a moderate (∼15%) increase of dP/dt which suggests an augmentation of active state intensity. Evidence is presented to suggest that this increase of dP/dt is based upon an increase in membrane Ca++ concentration which occurs secondary to inhibition of active Na+ transport. The alterations in ionic exchange and active state produced by variation of temperature are discussed in terms of a five-component control system.

/pdf/the-effects-of-temperature-upon-contraction-and-ionic-53rhencbvz.pdf

The Effects of Temperature upon Contraction and Ionic Exchange in Rabbit Ventricular Myocardium Relation to control of active state

The exchange of Ca45 was studied in dog myocardium by means of a newly developed perfusion technique whereby an excised papillary muscle was perfused through its own artery. This makes possible the sequential and simultaneous correlation of ionic flux with ventricular myocardial function with each muscle serving as its own control. Calcium exchange has the following characteristics: (a) The major component of calcium flux is independent of the frequency of contraction. It demonstrates a rapidly equilibrating phase (half-time, 4 to 6 minutes) and a more slowly equilibrating phase with a progressively decreasing rate constant. The flux characteristics of the more rapidly equilibrating compartment are determined by a factor or factors, in addition to simple diffusion, which increase the time required for this compartment to achieve a steady-state with respect to the vascular compartment. (b) A lesser component of exchange is stimulus-rate dependent and is characterized by an alteration in the rate of calcium turnover such that the altered influx: efflux ratio requires 20 to 25 minutes to achieve equilibrium. After this time, despite the higher stimulus rate, there is no evidence of change in total tissue calcium. (c) The initial rate of the transient response is approximately proportional to the change in stimulus rate.

/pdf/calcium-flux-in-the-mammalian-ventricular-myocardium-2oatiomxis.pdf

Calcium Flux in the Mammalian Ventricular Myocardium

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Specific Uncoupling of Excitation and Contraction in Mammalian Cardiac Tissue by Lanthanum Kinetic studies

The Effects of Temperature upon Contraction and Ionic Exchange in Rabbit Ventricular Myocardium Relation to control of active state

Calcium Flux in the Mammalian Ventricular Myocardium