The myocardial cell surface, its histochemistry, and the effect of sialic acid and calcium removal on its stucture and cellular ionic exchange.

Frank, J. S.; Langer, G. A.; Nudd, L.M.; Seraydarian, K.

doi:10.1161/01.res.41.5.702

Cited by 211 publications

(95 citation statements)

References 42 publications

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“…It remains uncertain as to whether the major portion of Ca involved in E-C coupling moves across the sarcolemma with each beat or whether a portion is released from internal sarcotubular sites by the mechanism of Ca-induced Ca release (21 plex (22). This complex contains large amounts of glycoprotein and glycolipid and carries a large quantity of negatively charged sites which are believed to represent the loci for Ca binding.…”

Section: Model For Myocardial Contractile Controlmentioning

confidence: 99%

Interspecies variation in myocardial physiology: the anomalous rat

Langer¹

1978

Environ Health Perspect

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The heart of the adult rat has long been recognized to be anomalous in at least two respects: an absent or negative inotropic response to an increase in rate of electrical stimulation (negative staircase); resistance to digitalis glycosides. The heart of the neonatal rat (less than 2 weeks old), on the other hand, demonstrates a markedly positive staircase and a large increase in force upon application of glycoside. It is significant that the action potential of the neonate ventricle demonstrates a prolonged plateau component which progressively decreases with age. The shortening of the plateau correlates with the disappearance of the positive staircase and glycoside responses. Previous studies indicated that a major factor contributing to the prolonged plateau of the neonate was a high level of sodium (Na) conductance. Thus transmembranous Na movement associated with excitation is considerably greater in the neonatal heart as compared to the heart of the adult rat. The higher level of intracellular Na would produce increased activity of a proposed sodium-calcium (Na-Ca) carrier. This is believed to mediate the augmented influx of Ca which is responsible for positive staircase and glycoside responses.Ventricular muscle from the hearts of most mammalian species demonstrates a prolonged plateau with maintenance of a "slow" channel for Na. It appears that in the rat this channel closes with age. It follows that there would be a reduced tendency for the adult rat heart to accumulate intracellular Na, [Na]i, when excitation frequency is increased or the Na pump is inhibited by digitalis. Since elevation of [Na]i is the stimulus for the proposed Na-Ca carrier, this system would not be activated, Ca influx would not increase and contractility would not be augmented.In many biological investigations it is the mutant organism or the anomalous species which frequently provides additional insights into basic mechanisms of function. Definition of the basis for an anomaly may further define the normal condition. In the area of mammalian myocardial physiology the rat has provided just such an anomalous condition. The rat heart demonstrates anomalies with respect to its action potential (1, 2), forcefrequency response (1-3), ionic exchange parameters (2, 4-6) and response to digitalis glycosides (2,7,8). Investigation of these characteristics has provided further insight into fundamental properties of myocardial function not only in the rat but in other mammalian species.I will first review the anomalies and then attempt to correlate them in such a manner as to indicate how the information has provided further definition of a model for control of myocardial force development.

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Section: Model For Myocardial Contractile Controlmentioning

confidence: 99%

Interspecies variation in myocardial physiology: the anomalous rat

Langer¹

1978

Environ Health Perspect

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“…Langer and his co-workers have found that removal of sialic acid from cultured myocardial cell surface by treatment with neuraminidase produces an enhancement of the Ca2" permeability of the membrane (Frank et al, 1977;Langer et al, 1979;. This observation suggested that the glycocalyx might in some way regulate the calcium ions which participate in the contractile response.…”

Section: Introductionmentioning

confidence: 98%

Inotropic effects of Ca²⁺ channel agonist and antagonists in neuraminidase‐treated left atria of rats

Hattori

Hazama

Kanno

et al. 1986

British J Pharmacology

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1 The effects of removal of sialic acid from cardiac sarcolemma on contractile functions and on inotropic responses to Ca2" channel agonist and antagonists were investigated in rat left atria.2 About 64% ofthe total sialic acid content of the left atria was removed during a 90 min exposure to neuraminidase (2 u ml ').3 The removal of sialic acid neither affected the development of twitch tension induced by stimulation at a frequency of0.5 Hz, nor altered the interval-dependent changes in contractility such as the force-frequency relationship and post rest contractions.4 The positive inotropic effects produced by isoprenaline, and by an increase in extracellular Ca2" concentration were the same in the neuraminidase-treated preparations as those in the untreated preparations. Bay K 8644, a Ca2+ channel agonist, induced an increase in conractility in the neuraminidase-treated preparations comparable to that in the untreated ones. 5 Neuraminidase treatment significantly attenuated the negative inotropic effects of verapamil and diltiazem, whereas it had no effect on that of nifedipine. 6 The results indicate that sialic acid removal modifies neither the basal contractile functions nor the positive inotropism which is associated with an enhancement of the slow inward Ca2' current.However, sialic acid, which constitutes the glycocalyx of the cardiac sarcolemma, may be involved in the mechanism of the Ca2+ channel antagonistic actions of verapamil and diltiazem, but not that of nifedipine. Thus, our results provide pharmacological evidence that verapamil and diltiazem behave differently from the dihydropyridine compounds.

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“…Coronary perfusion with a calcium-free solution results in the development of an electromechanical dissociation (Mines, 1913), but may in addition lead to an increase of the sarcolemmal permeability to calcium (Frank et al, 1977). As a consequence, reperfusion of the heart with calcium-containing solution results in a massive influx of calcium into the cells, followed by exhaustion of tissue high-energy phosphates, the rapid onset ol myocardial contracture, massive release of cell constituents, and extensive uItrastructural damage (Zimmerman et al , 1967;Boink et al, 1976;Hearse et al , 1978).…”

Section: Introductionmentioning

confidence: 99%