Release of noradrenaline from the cat spleen by potassium

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.

Section: Discussionmentioning

confidence: 99%

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

“…In addition, the observation that the evoked release of noradrenaline is potentiated in a sodium-free medium (Kirpekar & Wakade, 1968a) suggests that a competition between sodium and calcium ions may exist at the sympathetic nerve endings to modulate the release of noradrenaline. Competition between these ions has been observed in the contraction of the heart (Luttgau & Niedergerke, 1958) and the release of acetylcholine at cholinergic nerve endings (Birks, Burstyn & Firth, 1968).…”

Section: Introductionmentioning

confidence: 99%

“…The spontaneous release of endogenous noradrenaline in a sodium-deficient medium may be attributed to the failure of the uptake mechanism, since the transport mechanism for the uptake of exogenous catecholamine, and presumably the uptake of endogenous noradrenaline, is mediated by a specific sodium-dependent carrier mechanism (Iversen & Kravitz, 1966;Gillis & Paton, 1967;Kirpekar & Wakade, 1968a) located in the axonal membrane. In addition, the observation that the evoked release of noradrenaline is potentiated in a sodium-free medium (Kirpekar & Wakade, 1968a) suggests that a competition between sodium and calcium ions may exist at the sympathetic nerve endings to modulate the release of noradrenaline.…”

Section: Introductionmentioning

confidence: 99%

Release of noradrenaline from the cat spleen by sodium deprivation

Garcı́a

Kirpekar

1973

Self Cite

“…The net fractional release obtained with 10 mM 4-AP amounted to 22 and 28% in 2.5 and 0 Ca"+, respectively (P = 0.05). (Kirpekar & Misu, 1967;Kirpekar & Wakade, 1968 Effect oftetrodotoxin on tetraethylammonium-induced tritium release…”

Section: Incubation and Perfusion Solutionsmentioning

confidence: 99%

Ion dependence of the release of noradrenaline by tetraethylammonium and 4‐aminopyridine from cat splenic slices

Ceña¹,

Garcı́a

González-García³

et al. 1985

1 Cat splenic slices prelabelled with [3H]-noradrenaline were incubated in oxygenated Krebsbicarbonate solution at 37°C, and the spontaneous total 3H release into different incubation media monitored. In normal Krebs bicarbonate solution, the spontaneous tritium fractional release amounted to 3.7% of the tissue radiactivity content per 5 min collection period. 2 Tetraethylammonium (TEA) increased spontaneous transmitter release in a concentrationdependent manner; the release was maximal at 30 mM and was 3.5 times the basal release. 3 4-Aminopyridine (4-AP) also enhanced the spontaneous release of tritium. The response increased linearly with 4-AP concentration (1-10 mM). With 10 mM 4-AP, the release was as much as 6 times the basal transmitter release. Guanidine was much less potent than either TEA or 4-AP. 4 The secretory response to TEA or 4-AP was little affected by changes in external Ca2", Mg2+, Na+, Cl-, H2PO4 or by tetrodotoxin. 5 However, transmitter release evoked by TEA or 4-AP strongly depended upon the concentration of HCO3-of the incubation solution; in fact, the secretory response varied almost linearly between I and 25 mM HCO3 . 6 The mechanisms underlying these effects are probably related to the well-known ability ofTEA and 4-AP to block K+ conductance that would cause depolarization of the splenic sympathetic nerve terminals. The HCO3-requirements for the secretory response are probably related to the ability of C02/HCO3-solutions to mobilize and release Ca2+ from intracellular organelles.