Release of noradrenaline from the cat spleen by sodium deprivation

Garcı́a, Antonio G.; Kirpekar, S. M.

doi:10.1111/j.1476-5381.1973.tb08200.x

Cited by 82 publications

(26 citation statements)

References 29 publications

(36 reference statements)

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“…The result is consistent with data presented by Garcia and Kirpekar (6) in the cat spleen. On the other hand, it has been reported that in the rat heart, increases in the release and decreases in the stores of 3H-noradrenaline induced by sodium deprivation especially when replaced with choline,…”

supporting

confidence: 83%

Effects of Calcium and Guanethidine on Noradrenaline Output Induced by Sodium Reduction in Rabbit Atria

Misu

Hosotani

Nakashima

et al. 1977

Japanese Journal of Pharmacology

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supporting

confidence: 83%

Effects of Calcium and Guanethidine on Noradrenaline Output Induced by Sodium Reduction in Rabbit Atria

Misu

Hosotani

Nakashima

et al. 1977

Japanese Journal of Pharmacology

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“…Tissues lose their noradrenaline content when exposed to a lowsodium environment (Kirpekar & Wakade, 1968a;Bogdanski & Brodie, 1969;Garcia & Kirpekar, 1973). Experiments carried out to see if bretylium was released from the sympathetic nerve terminals by exposure to sodium-free medium clearly demonstrated that like noradrenaline, bretylium was released leading to an impairment of the ability of the tissue to retain [3H] -noradrenaline.…”

Section: Discussionmentioning

confidence: 99%

“…Ten min after the last washout the control preparation was exposed to bretylium (20;ig/ml for 5 minutes). (Kirpekar & Wakade, 1968a;Bogdanski & Brodie, 1969;Garcia & Kirpekar, 1973 (Figure 5, column B). On the other hand, in the half atrium treated with bretylium in normal Krebs, and then switched to sodium-free (sucrose) Krebs, retention of [ 3 H] -noradrenaline was also markedly decreased ( Figure 5, column C).…”

Section: Effect Of Potassium Deprivation On the Abili7 Of Bretylium mentioning

confidence: 99%

Influence of Cocaine and Sodium on Bretylium Uptake by Reserpine‐treated Guinea‐pig Left Atrium

Garcı́a¹,

Sánchez‐García²

1975

British J Pharmacology

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1The effects of cocaine and sodium on bretylium uptake into sympathetic nerve terminals were investigated in the reserpine-treated guinea-pig left atrium. The ability of bretylium pretreatment to increase the retention of noradrenaline was used as an index of bretylium uptake. Such increased retention has been assessed both by direct measurement and by the ability of tyramine to produce an inotropic response. 2 The restoration of the response to tyramine after incubation with noradrenaline was abolished when the atrium was pretreated with bretylium in the presence of cocaine. When bretylium was added before cocaine, or when ca-methyl-noradrenaline (not a substrate for monoamine oxidase) was used for incubation, the responses to tyramine were restored in the normal way. 3 Bretylium greatly enhanced the retention of [3 HI-noradrenaline; when bretylium was added in the presence of cocaine, [3HI -noradrenaline retention was severely impaired. 4 Pretreatment with bretylium in a low-sodium (25 mM) or sodium-free medium significantly decreased the retention of [ 3HI -noradrenaline, as compared with the control.5 Potassium deprivation did not modify the enhanced retention of [3 H I -noradrenaline induced by bretylium pretreatment. 6 Bretylium was released from the nerve terminals by exposure of the preparation to a sodium-free medium or to a solution containing calcium 50 mM, leading to a considerable decrease in 3H I -noradrenaline retention.7 The results are consistent with the view that both cocaine and sodium deprivation block the uptake of bretylium by the adrenergic nerve terminals, and that bretylium is probably taken up by a mechanism similar to or identical with the uptake system for noradrenaline and other amines.

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“…The major mechanism involved in this increase in the output of noradrenaline seems to be an inhibition of the retention rather than that of the reuptake, because guanethidine, a potent inhibitor of the uptake (Hertting, Axelrod & Patrick, 1962), did not potentiate the efflux induced by low sodium. Garcia & Kirpekar (1973) demonstrated that the various procedures which are known to inhibit Na+, K+-activated ATPase or the sodium potassium pump, induce the efflux of noradrenaline. However, the present result, showing that guanethidine inhibits the output of noradrenaline induced by low sodium, is not explicable in terms of the activation of this enzyme in the adrenergic nerve endings because the drug does not modify the myocardial transport ATPase activity (Misu & Nishio, 1978).…”

Section: Resultsmentioning

confidence: 99%

Prevention by Guanethidine Analogues of Output of Noradrenaline Induced by Sodium Reduction in Rabbit Ventricular Slices

Hosotani

Misu

1978

British J Pharmacology

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The prevention by guanethidine and related agents of the output of noradrenaline induced by low sodium was investigated in rabbit ventricular slices. When external NaCl was reduced, the output of noradrenaline into the medium collected at 30 min intervals, increased and the endogenous levels decreased. These changes induced by replacing sodium with sucrose or choline were not affected either by the omission of calcium and addition of 0.5 mm ethylene glycol‐bis(aminoethyl‐ether)N,N,N′,N′ tetra‐acetic acid (EGTA) or by an increase in the calcium concentration to 10 mm 30 min before sodium deprivation. Guanethidine 4 × 10−6 and 4 × 10−5m and 4–7‐exo‐methylene‐hexahydroisoindoline‐ethyl guanidine (No. 865‐123) 4 × 10−5 to 8 × 10−4m inhibited, in a dose‐dependent manner, increases in output of noradrenaline induced by reduction of sodium to 18 mm, while guanethidine 8 × 10−5m and high doses of bretylium produced no inhibition: the latter two released noradrenaline. The inhibitory actions of guanethidine 4 × 10−5m and No. 865‐123 4 × 10−4m were prevented by tetracaine 3.3 × 10−4m, which per se did not modify the output of noradrenaline induced by 18 mm sodium. Accumulation of guanethidine and No. 865‐123 in ventricular slices was greater than that noted in striated muscle slices and was dose‐, time‐ and temperature‐dependent. Tetracaine 3.3 × 10−4m did not prevent the accumulation of guanethidine 4 × 10−5m and No. 865‐123 1.1 × 10−6 to 4 × 10−4m. The guanidine derivatives appear to increase the permeability of adrenergic nerve endings to sodium ions.

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Release of noradrenaline from the cat spleen by sodium deprivation

Cited by 82 publications

References 29 publications

Effects of Calcium and Guanethidine on Noradrenaline Output Induced by Sodium Reduction in Rabbit Atria

Effects of Calcium and Guanethidine on Noradrenaline Output Induced by Sodium Reduction in Rabbit Atria

Influence of Cocaine and Sodium on Bretylium Uptake by Reserpine‐treated Guinea‐pig Left Atrium

Prevention by Guanethidine Analogues of Output of Noradrenaline Induced by Sodium Reduction in Rabbit Ventricular Slices

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