Stimulation of renal gluconeogenesis by verapamil and D-600

Gordon, Edwin E.; Ferris, Robert K.

doi:10.1016/0006-2952(77)90251-9

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…However, this cannot be so since gluconeogenesis from succinate and 2-oxoglutarate, as well as from lactate, is also increased with increasing Ca'+ (Kurokawa & Rasmussen, 1973;Alleyne et al, 1973), yet compound D-600 influences gluconeogenesis in a different manner with each of these substrates (see below). Furthermore, Gordon & Ferris (1977) have shown that verapamil has no effect on the gross Ca2+ content of renal tubules. Substrate and nutritional dependence of the effect of compound D-600 on gluconeogenesis Gordon & Ferris (1977) reported that 100puMcompound D-600 increased gluconeogenesis from [Ca2+1 (mM) Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, Gordon & Ferris (1977) have shown that verapamil has no effect on the gross Ca2+ content of renal tubules. Substrate and nutritional dependence of the effect of compound D-600 on gluconeogenesis Gordon & Ferris (1977) reported that 100puMcompound D-600 increased gluconeogenesis from [Ca2+1 (mM) Fig. 8.…”

Section: Resultsmentioning

confidence: 99%

“…50% in tubule fragments isolated from 24-h-starved rats. The experiments shown in Table 1 was therefore performed to ascertain whether the difference in compound D-600 actions between our findings and those of Gordon & Ferris (1977) was attributable to differences in nutritional status or to differences in gluconeogenic substrate. Table 1 shows that, in our hands, the effect of compound D-600 differed considerably with the substrate used.…”

Section: Resultsmentioning

confidence: 99%

“…Verapamil and its methoxy derivative, compound D-600, are of interest since they inhibit Ca2+-associated activities in various tissues (see review by Singh, 1978). However, there have only been two brief reports dealing with the effects of these agents on gluconeogenesis; one in liver where compound D-600 had little effect on basal or on glucagon-and adrenaline-stimulated gluconeogenesis from lactate (Fain et al, 1975); the other in renal cortex where verapamil and compound D-600 stimulated gluconeogenesis from succinate or 2-oxoglutarate (Gordon & Ferris, 1977). It was therefore of interest to investigate the effect of compound D-600 on the stimulation of renal gluconeogenesis by a-adrenergic agents.…”

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confidence: 99%

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Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

Saggerson¹,

Carpenter²

1980

Biochemical Journal

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1. Tubule fragments were isolated from renal cortex of fed rats and glucose formation was measured after incubation with 5 mM-sodium lactate. 20 Compound D-600 (10-100 microM) decreased gluconeogenesis from lactate. This inhibition of the process by compound D-600 increased with increasing extracellular Ca2+ concentration, was overridden by noradrenaline and diminished by starvation for 24 h. 3. Inhibition of lactate-supported gluconeogenesis by compound D-600 was not prevented by the alpha 1-adrenoceptor antagonist thymoxamine. 4. Compound D-600 had little effect on gluconeogenesis from 2-oxoglutarate and increased gluconeogenesis from succinate. 5. Compound D-600 opposed stimulation of gluconeogenesis by noradrenaline or oxymetazoline (a selective alpha-adrenoceptor agonist) in a manner suggesting that compound D-600 is an alpha-adrenoceptor blocker. Oxymetazoline was more sensitive than noradrenaline to blockade by both compound D-600 and by the conventional alpha-adrenoceptor antagonist phentolamine. Noradrenaline became more sensitive to blockade by compound D-600 when extracellular Ca2+ was decreased. 6. Compound D-600 did not block stimulation of gluconeogenesis by angiotensin or cyclic AMP.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

Saggerson¹,

Carpenter²

1980

Biochemical Journal

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“…The protection of the ischemic kidney by benidipine could be attributed to this in hibition by benidipine of Ca-overload. The existence of voltage-dependent slow calcium channels in non-exitable tissues remains to be established (24), and Gordon and Ferris (25) reported that neither verapamil nor methoxy verapamil influences the net influx or efflux of calcium in kidney tubules studied in vitro. Thus, it is still uncertain whether benidipine prevented calcium overload via the inhibition of voltage-dependent calcium channels or via the other mechanism.…”

Section: Discussionmentioning

confidence: 99%

Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.

Karasawa

Kubo

1990

Jpn.J.Pharmacol

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Calcium Channel Blockade in Experimental Aminoglycoside Nephrotoxicity

Watson

Gimenez

Klassen

et al. 1987

The Journal of Clinical Pharma

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Calcium channel blocker therapy has proved protective in certain models of ischemic-induced acute renal failure. This effect may be related to the prevention of calcium influx into injured cells or by the vasodilatory effects of verapamil that may result in an improvement in renal blood flow. In the current study, the effect of verapamil treatment on the development of renal insufficiency and renal tissue calcium accumulation following aminoglycoside administration was investigated. The degree of functional damage and cortical tissue calcium accumulation after six or nine days of gentamicin administration (120 mg/kg body weight/day) was not significantly different in rats whose drinking water contained verapamil (10 mg/100 cc) than corresponding values in control animals. The tissue calcium accumulation correlated with the degree of reduction of creatinine clearance and probably reflects the extent of lethal tubular cell injury.

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Stimulation of renal gluconeogenesis by verapamil and D-600

Cited by 7 publications

References 25 publications

Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.

Calcium Channel Blockade in Experimental Aminoglycoside Nephrotoxicity

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