Increase in free Ca2+ in muscle after exposure to CO2

Lea, T. J.; Ashley, C. C.

doi:10.1038/275236a0

Cited by 120 publications

(46 citation statements)

References 18 publications

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“…These studies followed those of Baker & McNaughton (1977) who showed that a decrease in pHi in squid axons reduced Ca efflux and those of Baker & Honerjiager (1978) where it was claimed that a decrease in pHi lowered [Ca]i. This claim has not been substantiated by measurements in barnacle (Lea & Ashley, 1978) nor does it agree with the study of cited above.…”

Section: Introductionmentioning

confidence: 39%

“…An experiment is shown in Fig. 8 Lea & Ashley (1978) have noted that aequorin-measured resting glow in barnacle fibres is enhanced by treating the fibres with CO2 and inhibited by the application of NH4+ to the fibre, treatments known to respectively acidify or alkalinize the myoplasm. A similar result has been described in squid giant axons by exchange (Baker & McNaughton, 1977) and that Ca entry might change pHi (Meech & Thomas, 1977;, it seemed useful to examine the way that axoplasm might respond to an alkaline challenge from [NH4]0 both by measuring the response of a glass electrode and that of a pH dye (phenol red is induced rapidly by the use of substances such as external NH4+, it is of some interest to know whether the glass electrode and the spectrophotometric measurement of [H+] give the same value as a function of time.…”

Section: Methodsmentioning

confidence: 99%

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Effects of internal sodium and hydrogen ions and of external calcium ions and membrane potential on calcium entry in squid axons.

Mullins¹,

Tiffert²,

Vassort³

et al. 1983

The Journal of Physiology

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SUMMARY1. Squid giant axons were impaled with electrodes to measure pNai, pHi, Em, and were injected with either aequorin or arsenazo III to measure [Ca] [Ca]. is 3 mM.4. The introduction of 2 mM-CN into the sea water bathing the axon does not affect the response to depolarization nor does the destruction of most of the ATP in the axon following the injection of apyrase.5. If axons are microinjected with phenol red rather than arsenazo, the entry of Ca produces an acidification in the peripheral parts ofthe axoplasm. Other experiments measuring [Ca]i show that Ca entry is strongly inhibited by a decrease in pHi.6. Making sea water alkaline with pH buffers scarcely affects the Ca entry induced by depolarization; making axoplasm alkaline by adding NH4+ to sea water greatly enhances Ca entry by Na/Ca exchange and also enhances the ability of axoplasmic buffers to absorb Ca.

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Section: Introductionmentioning

confidence: 39%

Section: Methodsmentioning

confidence: 99%

Effects of internal sodium and hydrogen ions and of external calcium ions and membrane potential on calcium entry in squid axons.

Mullins¹,

Tiffert²,

Vassort³

et al. 1983

The Journal of Physiology

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“…These differential effects may reflect the difference between simple acidic inhibition of Ca 2 + influx by changes in ECF pH (Weiss, 1966 ;Morganstern et aI ., 1972;Landau and Nachsen, 1975 ;Pickard et aI ., 1976) and the effect on intracellular binding of Ca 2 + by changes in intracellular pH produced initially by CO2 (Pickard, 1976) . The latter phenomenon has been described in other tissues, but the situation is complex (Fabiato and Fabiato, 1978;Lea and J Cereb Blood Flow Metabol, Vol. I, No.…”

Section: Clinical Significance Of Cerebral Arachidonate Metabolismmentioning

confidence: 98%

Role of Prostaglandins and Arachidonic Acid Derivatives in the Coupling of Cerebral Blood Flow to Cerebral Metabolism

Pickard

1981

J Cereb Blood Flow Metab

174

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“…Extracellular acidosis causes a sustained contractile response in isolated aortas from spontaneously hypertensive and control normotensive rats [10]. Intracellular acidosis increases constrictor tone, in association with simultaneous increases in cytosolic free Ca 2+ , as reported in barnacle and frog muscle fibres [11,12]. We and others, moreover, have demonstrated that plasma levels of CF6 were increased in patients with hypertension and diabetes [13,14].…”

Section: Introductionmentioning

confidence: 95%

Coupling factor 6-induced activation of ecto-F1Fo complex induces insulin resistance, mild glucose intolerance and elevated blood pressure in mice

Osanai

Tanaka

Magota³

et al. 2011

Diabetologia

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Aims/hypothesis Despite advances in pharmacological treatments, diabetes with hypertension continues to be a major public health problem with high morbidity and mortality rates. We recently identified a circulating peptide coupling factor 6 (CF6), which binds to the plasma membrane ATP synthase (ecto-F 1 F o complex), resulting in intracellular acidosis. We investigated whether overexpression of CF6 contributes to diabetes and hypertension by intracellular acidosis. Methods Transgenic mice overexpressing CF6 (also known as ATP5J) were generated, and physiological, biochemical and molecular biology studies were performed. Results CF6 overexpression elicited a sustained decrease in intracellular pH in tissues (aorta, kidney, skeletal muscle and liver, with the exception of adipose tissue) that express its receptor, the β-subunit of ecto-F 1 F o complex. Consistent with the receptor distribution, phospho-insulin receptor β, phosphoinositide 3-kinase activity and the phospho-Akt1: total Akt1 ratio were all decreased in the skeletal muscle and the liver in transgenic compared with wild-type mice, resulting in a decrease of plasma membrane-bound GLUT4 and an increase in hepatic glucose production. Under a high-sucrose diet, transgenic mice had insulin resistance and mild glucose intolerance; under a high-salt diet, they had elevated blood pressure with increased renal RASrelated C3 botulinum substrate 1 (RAC1)-GTP, which is an activator of mineralocorticoid receptor. Conclusions/interpretation Through its action on the β-subunit of ecto-F 1 F o complex, which results in intracellular acidosis, CF6 plays a crucial role in the development of insulin resistance and hypertension. This finding might advance our understanding of the mechanisms underlying diabetes and hypertension, possibly also providing a novel therapeutic target against cardiovascular disease.

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Increase in free Ca2+ in muscle after exposure to CO2

Cited by 120 publications

References 18 publications

Effects of internal sodium and hydrogen ions and of external calcium ions and membrane potential on calcium entry in squid axons.

Effects of internal sodium and hydrogen ions and of external calcium ions and membrane potential on calcium entry in squid axons.

Role of Prostaglandins and Arachidonic Acid Derivatives in the Coupling of Cerebral Blood Flow to Cerebral Metabolism

Coupling factor 6-induced activation of ecto-F1Fo complex induces insulin resistance, mild glucose intolerance and elevated blood pressure in mice

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