Biomedical subjects
C P Bianchi
Publications and source records attributed to C P Bianchi.
Stimulation-enhanced 3-O-methylglucose efflux from the frog sartorius: kinetics and properties of the system.
The characteristics of the process by which contraction enhances glucose transport in the frog sartorius were studied. Electrical stimulation increased the permeability of muscles to 3-O-methylglucose (3-O-MeGlc), a nonmetabolizable glucose analogue, increasing efflux as well as uptake. Enhanced efflux was due to an increase in Vmax of the efflux process. A lactacidosis had no effect on basal 3-O-MeGlc efflux, and replacement of media Na+ with Li+ did not affect stimulation-induced uptake. Also, basal and stimulated uptake was not affected by 1 microM 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator. Lastly, N-carbobenzoxy-glycyl-L-phenylalaninamide, which inhibits insulin-enhanced, but not basal, glucose uptake in adipocytes, inhibited both basal and stimulated 3-O-MeGlc fluxes in the frog sartorius. From these findings, we conclude: (1) contraction and exercise enhance glucose transport in muscle by increasing the number of transporters in the plasma membrane, or their turnover, by an unknown process; and (2) basal glucose transport of muscle, unlike that of adipocytes, can not be distinguished from stimulated transport on the basis of its insensitivity to N-carbobenzoxyglycyl-L-phenylalaninamide.
Role of calcium channels of the sarcolemma and the sarcoplasmic reticulum in skeletal muscle functions.
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The George B. Koelle symposium on the cholinergic synapse.
The George B. Koelle Symposium on the Cholinergic Synapse described the early development of the importance of ACh as a transmitter at both cholinergic synapses of the CNS, ganglion and neuromuscular junction. While a great deal is known about the function of cholinergic transmission at the neuromuscular junction, the integrated role of cholinergic, nicotinic and muscarinic receptors in the overall process of CNS functions, i.e., behavior, motor control, abstract thinking, memory and speech remains as a challenge for future investigation. The architecture of the cholinergic synapse appears to be a dynamic process involving ARIA, Agrin and the various forms of ACh esterase. The regulation of gene expression and site directed localization of postsynaptic cholinergic receptor proteins during the life cycle involves the dynamic interactions of these agents with the postsynaptic membrane and postsynaptic gene express. The last two papers at the symposium dealt with the chemistry of the nicotinic receptor regulated channel involved in ACh binding and the consequent cationic channel conductional changes.
Trace metal (Cu and Zn) adaptation of organ systems of the American eel, Anguilla rostrata, to external concentrations of cadmium.
1. The impact of external cadmium on the concentrations of cadmium (Cd), copper (Cu) and zinc (Zn) in seven tissues of the American eel, Anguilla rostrata was investigated. Even after a week in freshwater with undetectable levels of Cd, the tissues of eels caught in fresh and/or brackish waters of the United States east coast contained Cd in kidney, liver, gut, and brain. 2. When the eels were exposed up to 16 weeks to low and high sublethal concentrations of Cd (75 and 150 micrograms/l, respectively), the highest tissue concentrations of Cd were found after two weeks of exposure. The accumulation was dose-related in all tissues studied except for the kidney. After 8 weeks of Cd exposure, the tissue levels of Cd were markedly reduced, and they were in a similarly low range after 16 weeks. At this time, the highest Cd concentrations were found in the gills and kidney. 3. After two weeks of Cd exposure, there was a drop of the tissue concentrations of Cu in liver and heart, and of Zn in gut and liver. The low concentrations of the two metals in other organs did not allow an evaluation of the Cd impact. After 16 weeks, the Cu concentrations in all tissues, with the exception of the liver, were similar to, or even higher than control levels. At the same time, Zn concentrations exceeded the control levels in heart and kidney of eels exposed to 75 and 150 micrograms Cd/l, respectively. 4. It is clear that some tissues of the eel are able to maintain or restore normal levels of Cu and Zn, up to 16 weeks, despite concomitant Cd accumulation.
Endogenous "ryanodine agonist" and hyperthermia.
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Bimodal operation of the ryanodine-sensitive transducer calcium channel.
Ryanodine binds to the transducer calcium channel complex that links depolarization of the transverse tubule to calcium release from the terminal cisternae during excitation-contraction coupling of skeletal muscle. Ryanodine exerts a bimodal action on the transducer calcium channel complex depending upon membrane potential and concentration. When the transmembrane potential is at resting level (-90 mV inside cell vs outside), low concentrations of ryanodine 10(-10) M to 10(-8) M favor calcium influx from outside which in turn causes calcium release from the terminal cisternae via calcium operated calcium channels. The leak from the terminal cisternae is insufficient to cause contraction but does cause a large increase in aerobic energy utilization by the Ca-ATPase of the sarcoplasmic reticulum. When the transmembrane potential is made more positive (-40 mV) the transducer channel is opened to the terminal cisternae of sarcoplasmic reticulum and is maintained in an open state by ryanodine allowing calcium efflux from the terminal cisternae to the sarcoplasm. At higher concentrations of ryanodine the transducer-calcium channel becomes open to the terminal cisternae and its store of ionized calcium leaks from the terminal cisternae in sufficient quantities to cause a contracture. The ryanodine-sensitive calcium transducer calcium channel operates in a bimodal manner. At low concentrations less than 10(-4) M the ryanodine-sensitive transducer calcium channel is open to the lumen of the T-tubule and allows calcium to flow in and trigger further calcium release. At higher concentrations the ryanodine-sensitive transducer channel opens to allow a calcium efflux from the terminal cisternae in sufficient quantities to cause contracture.
Steady state maintenance of electrolytes in the spinal cord of the frog.
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Regulation of aerobic metabolism of frog skeletal muscle by calcium, cyclic GMP and cyclic AMP.
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Calcium uptake and exchange in leg nerves of the crab 'Libinia emarginata'.
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Mode of action of veratridine on perfused frog ventricle.
Veratridine exerts a biphasic action on the perfused frog ventricle. The initial immediate response is a depression, which is maximal at 10(-10) M. The initial depression is followed by a late potentiation of contraction which is maximal at 10(-6) to 10(-7) M veratridine. Reduction of external calcium from 1.0 mM to 0.5 mM prevents the initial depression and allows only the potentiation of contraction to be observed. The force of contraction in 0.5 mM Ca2+ is increased by veratridine to 200% of the contraction observed at 1.0 mM Ca2+. The primary site for the enhancement of contraction in the frog ventricle by veratridine is the adrenergic nerve fibers whose increase in excitability leads to an increase in epinephrine release. The beta blocker sotalol at 10(-6) M prevents the increase in contractility by veratridine in 0.4 mM Ca2+. Calcium itself depressed potentiation of contractility by veratridine by stabilizing the adrenergic nerves and antagonizing the labilizing action of veratridine. The mode of action of veratridine on the frog ventricle is attributed to the enhancement of transmitter release from cholinergic and adrenergic nerve fibers.
Restoration of potassium-stimulated respiration of glycerol-treated muscle.
Agent that produced contracture in skeletal muscle, such as caffeine or K-depolarization, also caused an increased rate of oxygen consumption. Both of these functions are calcium dependent. In this study the respiratory response to K-depolarization and to caffeine was monitored in glycerol-treated and normal frog sartorius muscles. Although glycerol-treated muscle does not contract in response to K-depolarization, it does develop normal caffeine contractures. The respiratory response to both potassium and caffeine is greatly inhibited in glycerol-treated muscles. Pretreatment with dibutyryl cyclic AMP restored the respiratory response to normal levels in glycerol-treated muscle. Pretreatment with low levels of caffeine that had no effect on oxygen uptake markedly enhanced oxygen uptake with higher concentrations of caffeine and resulted in a normal respiratory response to K-depolarization even though there was no tension development. Caffeine had no effect on adenyl cyclase activity even at concentrations that markedly stimulated oxygen uptake. The data suggest that potassium stimulation of oxygen uptake in glycerol treated muscle is uncoupled by a defect in the formation of a cyclic nucleotide cofactor, rather than a defect in calcium influx.
Ca2+ concentration and interaction of long-lasting local anaesthetics with the squid axon membrane.
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Effect of isoproterenol and D-600 on calcium movements in rat myometrium.
The effects of two smooth muscle relaxants, isoproterenol and D-600, on calcium movements in rat myometrium were investigated. Both relaxants caused a nonspecific increase in 45-Ca efflux due to changes in mechanical tension but the additional net loss expected on the basis of previous studies with isoproterenol could not be demonstrated due to a high background of calcium exchange. Analysis of 45-Ca and 40-Ca residual in the muscle after efflux experiments and washing of the tissue in a Ca-deficient solution containing LaCl3 (2.0 mM) showed that the specific activity ratio 45-Ca/40-Ca was unaltered with isoproterenol and, thus, the net loss of calcium occurred equally from slowly and rapidly exchanging compartments. "Pulse label" experiments in which 45-Ca and either isoproterenol or D-600 were added simultaneously for a 2-minute period demonstrated that both relaxants decreased the 45-Ca space; however, the specific activity ratio 45-Ca/40-Ca in the tissue was reduced while 40-Ca remained unchanged in the presence of D-600. With isoproterenol, the 45-Ca/40-Ca ratio was increased while 40-Ca was reduced. These data support the hypothesis that isoproterenol stimulates a net efflux of calcium whereas D-600 inhibits the influx of calcium. Since previous studies have demonstrated that relaxants which increase cyclic3,5-adenosine monophosphate (cyclic AMP) (isoproterenol, dibutyryl cyclic AMP and papaverine) produce consistent decreases in tissue Ca but others (D-600) do not, it is concluded that relaxants which increase tissue cyclic AMP stimulate a net efflux of calcium but other antagonists may act by inhibiting calcium influx into rat myometrium.
Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat.
Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.