Release of noradrenaline by splenic nerve stimulation and its dependence on calcium

Abstract

SUMMARY1. Cat spleens were perfused with Krebs bicarbonate solution using a constant flow pump. The amount of noradrenaline released during splenic nerve stimulation was measured at various frequencies. The dependence of noradrenaline release on the ionic composition of perfusion medium was also determined.2. The effect of frequency of stimulation on the output of noradrenaline was studied in both normal and phenoxybenzamine treated cats. In normal cats, the output was 0 33 ng/stimulus at 10/sec, whereas it was 1-21 ng/ stimulus at 30/sec. In phenoxybenzamine-treated cats, the maximum output of noradrenaline of 4 ng/stimulus was obtained at 5 or 10/sec. Higher or lower frequencies of stimulation produced lower output.3. In both normal and phenoxybenzamine treated cats, removal of calcium from the perfusing medium nearly abolished the release of noradrenaline in response to nerve stimulation. Replacement of calcium restored the noradrenaline release. The noradrenaline output/stimulus was linearly related to the log of the external calcium concentration.4. Increasing the concentration of magnesium to (10-20 mM) reduced the noradrenaline output. This depressant effect of magnesium was partially antagonized by increasing the calcium concentration of the perfusion solution.5. Divalent alkali metal earths such as barium and strontium were able to substitute for calcium. Barium substitution nearly doubled the noradrenaline output/stimulus and increased the pressor activity of the samples taken just before nerve stimulation.6. Removal of potassium from the perfusion fluid or lowering the sodium concentration to 50 mm had little effect on the release of noradrenaline. Lowering the sodium concentration to 37X5 mm or less usually abolished the noradrenaline output; this effect is attributed to blockade of nerve conduction. 220 S. M. KIRPEKAR AND Y. MISU 7. It is suggested that depolarization of post-ganglionic sympathetic nerve terminals may increase the influx of calcium ions which in turn leads to the release of noradrenaline from the nerve terminals.

Release of noradrenaline from the cat spleen by sodium deprivation

“…The effect of calcium on the efflux of noradrenaline induced by sodium deprivation Since calcium is required for the evoked release of noradrenaline (Hukovic & Muscholl, 1962;Kirpekar & Misu, 1967) from sympathetically innervated tissues, experiments were done to determine the effect of calcium removal on noradrenaline loss induced by sodium deprivation. Figure 3a shows that removal of calcium alone, or removal of calcium plus addition of EGTA (0-1 mM), did not have any appreciable effect on the efflux of noradrenaline.…”

An Electrophysiological Analysis of the Effects of Morphine on the Calcium Dependence of Neuromuscular Transmission in the Mouse Vas Deferens

“…Although the motor response of the vas deferens during short trains of impulses is reduced only 66% following a 97% reduction of the NA levels with reserpine (Marshall, Nasmyth & Shepperson, 1978), this may be due to reserpine reversing the normal depression in ej.p. amplitude which occurs during a high-frequency train to facilitation (see Figure 2 in Bennett & Middleton, 1975a (Dearnaley & Geffen, 1966;Kirpekar & Misu, 1967;Kopin, Breese, Krauss & Weise, 1968;Stjarne & Wennmalm, 1970;Stjarne, 1973) and relative changes in the amplitude of the e.j.p. (Bennett, 1973a;Bennett & Florin, 1975).…”

Release of noradrenaline and dopamine by nerve stimulation in the cat spleen perfused with 3H‐dopamine

“…The abdomen was opened by a midline incision, and the stomach, adrenals, intestines and colon were removed. The spleen was isolated and perfused in situ with Krebs bicarbonate solution at a constant rate of about 7 ml/min, at 350 C (Kirpekar & Misu, 1967). 3H-dopamine (280 mCi/mmol) was infused into the splenic artery for 90 min at a constant rate of 20 ng/min in a volume of 0 05 ml by placing a cannula in the hepatic artery so that the tip of the cannula was at the junction of the hepatic artery with the main coeliac artery.…”