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

Garcı́a, Antonio G.; Sánchez‐García, P.

doi:10.1111/j.1476-5381.1975.tb07356.x

Cited by 4 publications

(6 citation statements)

References 14 publications

(21 reference statements)

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“…The uptake of [3H]NA was more prominent in P1 segments (proximal to the ligature) that in DI segment (distal to the ligature) and seems to be very specific, since cholinergic nerves and fragments of peritoneum, of weight and size similar to hypogastric nerves, took up and retained [3H]NA in much smaller amounts and this uptake was not blocked by cocaine. Reserpine not only decreased the NA content ofnerves but also diminished the net uptake of [3H]NA, probably by reducing its retention, as a consequence of intraneuronal deamination by monoamine oxidase as occurs in other tissues (Furchgott & Sanchez-Garcia, 1968;Garcia & Sanchez-Garcia, 1975). Our results also show that 6-hydroxydopamine, after collagenase treatment of nerves, markedly decreased the net uptake of [3H]NA.…”

Section: Discussionsupporting

confidence: 72%

“…It is well known that cocaine blocks NA uptake by noradrenergic nerve terminals (see MacMillan, 1959;Whitby et al 1960;Muscholl, 1961;Iversen, 1967;Furchgott & Sanchez-Garcia, 1968;Garcia & Sanchez-Garcia, 1975). The results of the present experiments also showed that cocaine markedly diminished the [3H]NA uptake both in unligated and ligated hypogastric nerve trunks but not in vagus nerve and peritoneum, indicating that the uptake of [3H]NA into the sympathetic nerve takes place through a carrier similar to the U1 uptake system described in the nerve terminals.…”

Section: Presence Of An Na Carrier In Ligated Nervesmentioning

confidence: 99%

“…Table 1 shows that the reduction of [3H]NA net uptake was parallel in atria and hypogastric nerves. It is known that reserpine does not alter the capacity of adrenergic tissues to take up NA (Lindmar & Muscholl, 1964;Iversen et al 1965;Gillespie & Kirpekar, 1965;Furchgott & Sainchez-Garcia, 1968;Garcia & Sanchez-Garcia, 1975) but it does somehow inactivate the mechanism for active incorporation of NA into the storage vesicles, exposing the amine present in the cytoplasm to the inactivation by monoamine oxidase (Furchgott & Sanchez-Garcia, 1968 Collagenase removes a barrier that limits the access of polar molecules to the axons of ligated nerves 6-Hydroxydopamine is a neurotoxin that selectively destroys sympathetic nerve terminals (Tranzer & Thoenen, 1967) and decreases the net uptake of [3H]NA by adrenergic nerve terminals. The results of our experiments have also demonstrated that an acute, in vitro treatment with 6-hydroxydopamine in the presence of collagenase markedly decreased the net uptake of [3H]NA by hypogastric nerves.…”

Section: Presence Of An Na Carrier In Ligated Nervesmentioning

confidence: 99%

“…This uptake system (U1) is located on noradrenergic nerve terminals (Whitby, Axelrod & Weil-Malherbe, 1961;Iversen, 1963), blocked by cocaine (Whitby, Hertting & Axelrod, 1960;Muscholl, 1961;Furchgott, Kirpekar, Rieker & Schwab, 1963;Furchgott & SanchezGarcia, 1968;Garcia & Sanchez-Garcia, 1975), by various sympathomimetic amines, by tricyclic antidepressants and by the haloalkylamine phenoxybenzamine (see Iversen, 1967). It is also well known that pre-treatment with reserpine depletes the catecholamine content of adrenergically innervated tissues (see Carlsson, 1966) and that 6-hydroxydopamine is a neurotoxin that markedly decreases the NA content of adrenergic nerve terminals (Stone, Stavorsky, Ludden, Wengler, Ross, Totaro & Porter, 1963).…”

mentioning

confidence: 99%

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Presence of a noradrenaline uptake system on a ligated cat sympathetic nerve.

Ceña¹,

Garcı́a²,

Pi³

et al. 1986

The Journal of Physiology

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SUMMARY [3H]noradrenaline ([3H]NA) uptake studies were carried out in cat hypogastric nerves ligated in vivo, 2 cm distal to the inferior mesenteric ganglion, for different time periods. Atria from the same animals served as controls to determine the uptake of the amine by the U1 uptake system present in noradrenergic nerve terminals.2. The net uptake of [3H]NA by hypogastric nerves increased with time of ligation, reaching a maximum 24 h after ligation in the segment of nerve immediately proximal to the ligature (PI segment, neurosome). No further increase in uptake was observed at 48 or 72 h. Segments distal (D1) to the ligature also retained significant amounts of [3H]NA. In both cases the uptake was blocked by cocaine (3 #M).3. Reserpine pre-treatment (2 mg/kg I.M.) markedly decreased the endogenous NA content to 1-2 % ofuntreated cats and the net uptake of [3H]NA was lowered to 25 % both in cat hypogastric nerve and atria. The uptake was further decreased in the presence of cocaine (3 #M).4. 6-Hydroxydopamine (100 ,IM) did not modify the [3H]NA uptake by ligated cat hypogastric nerves but almost abolished the [3H]NA net uptake by right atria from the same animals. After collagenase pre-treatment (0 05 % for 15 min) the net uptake of [3H]NA was not altered in the atrium. However, collagenase-pre-treated ligated nerves, took up almost twice as much [3H]NA; under these conditions, 6-hydroxydopamine produced a marked decrease in [3H]NA net uptake. These data suggest the presence in the perineurium of a diffusion barrier for very polar substances, including 6-hydroxydopamine.5. In conclusion, our data demonstrate that the cat hypogastric nerve ligated in vivo has a cocaine-sensitive system for NA uptake which resembles the NA uptake mechanism (U1) present in noradrenergic nerve terminals. Our data further support the view that the ligated cat hypogastric nerve (neurosome) could be considered as a model of noradrenergic nerve terminal free of effector cell.

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Section: Discussionsupporting

confidence: 72%

Section: Presence Of An Na Carrier In Ligated Nervesmentioning

confidence: 99%

Section: Presence Of An Na Carrier In Ligated Nervesmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Presence of a noradrenaline uptake system on a ligated cat sympathetic nerve.

Ceña¹,

Garcı́a²,

Pi³

et al. 1986

The Journal of Physiology

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“…The uptake was saturable with an apparent Km of 3 x 10-6 M. The uptake was inhibited by amphetamine, norepinephrine, desmethylimipramine, cocaine, guanethidine, low sodium and ouabain. GARCiA and SANCHEZ-GARCiA (1975) using indirect methods studied the uptake of bretylium in reserpine-treated, guinea-pig atria. Cocaine and low sodium greatly reduced the retention of bretylium.…”

mentioning

confidence: 99%

Adrenergic Neuron Blocking Drugs

Maxwell¹,

Wastila²

1977

Antihypertensive Agents

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

Cited by 4 publications

References 14 publications

Presence of a noradrenaline uptake system on a ligated cat sympathetic nerve.

Presence of a noradrenaline uptake system on a ligated cat sympathetic nerve.

Adrenergic Neuron Blocking Drugs

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

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