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Biomedical subjects

Y Misu

Publications and source records attributed to Y Misu.

178 records · Page 10Linked to original sources
PubMed1967

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

1. 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 37.5 mM or less usually abolished the noradrenaline output; this effect is attributed to blockade of nerve conduction.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.

Animals↗
PubMedDate not supplied

Presynaptic beta-adrenoceptors.

The existence of facilitatory presynaptic beta-adrenoceptors has been shown in approximately 30 tissues of 6 different species including human. A positive feed back loop for further release of the transmitter appears to be activated by an endogenous agonist, epinephrine, taken up and released as a cotransmitter with norepinephrine rather than norepinephrine itself released from peripheral noradrenergic nerve terminals. Presynaptic beta-adrenoceptors are mainly of a beta 2-subtype. Some beta 1-subtype receptors are also suggested. There coexist presynaptic beta 1- and beta 2-adrenoceptors in cat and rat hypothalamus. Higher sensitivity of peripheral presynaptic beta-adrenoceptors to isoproterenol may be implicated in the early development of hypertension in SHR. Epinephrine taken up and released initiates the development of hypertension in rats via activation of these receptors. Increased activation of these receptors by epinephrine may play a role in the development of essential hypertension. The antihypertensive action of beta-antagonists may be in part due to blockade of these facilitatory presynaptic beta-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Coexistence of presynaptic beta 1- and beta 2-adrenoceptors in splenic strips from young rats and betaxolol-induced beta 1-stereoselective antagonism.

The pharmacological properties of facilitatory presynaptic beta-adrenoceptors were characterized using three kinds of beta-agonists and antagonists in superfused strips from young Sprague-Dawley rats, loaded with [3H]noradrenaline. Isoproterenol (10(-9) M to 10(-7) M) concentration-dependently facilitated [3H] release evoked by transmural field stimulation at 5 Hz. Salbutamol (10(-8) M and 10(-7) M) and prenalterol (10(-8) M to 10(-6) M) also facilitated the stimulation-evoked [3H] release. Pretreatment with ICI 118,551 (10(-6) M) completely antagonized the concentration-facilitation curve for isoproterenol (10(-9) M to 10(-7) M). Atenolol (10(-6) M) antagonized only the isoproterenol (10(-9) M)-induced facilitation. dl-Betaxolol (10(-6) M) antagonized the isoproterenol (10(-9) M and 10(-8) M)-induced facilitation and the antagonistic action for isoproterenol (10(-8) M) was more marked than that of atenolol, whereas the same concentration of d-betaxolol produced no antagonism. Thus, presynaptic beta 1- and beta 2-adrenoceptors coexist on noradrenergic neurons innervating splenic strips of young rats. Betaxolol is a useful tool to characterize presynaptic beta 1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Stress-induced increases in adrenaline further activate tonically presynaptic beta-adrenoceptors in renal arteries from prehypertensive rats of spontaneously hypertensive strain.

The effects of cumulatively applied doses (10(-8) M, 10(-7) M and 10(-6) M) of dl-carteolol, a nonselective beta-antagonist, on stimulation-evoked [3H] release at 5 Hz for 40 sec, were studied in renal arteries isolated from prehypertensive 4 weeks old spontaneously hypertensive rats unexposed and exposed to swimming stress for 1 hr, and then loaded with [3H]-noradrenaline. Carteolol, at 10(-8) M and 10(-7) M, produced no effect and at 10(-6) M it slightly inhibited the evoked [3H] release in the arteries from control spontaneously hypertensive rats. Carteolol, 10(-8) M to 10(-6) M, consistently inhibited the evoked [3H] release in renal arteries from spontaneously hypertensive rats exposed to stress and this inhibition differed from no effect, at 10(-8) M and 10(-7) M, and was greater than that at 10(-6) M in the arteries from control spontaneously hypertensive rats. Swimming stress increased the endogenous contents of adrenaline and dopamine in renal arteries without altering the level of noradrenaline. In conclusion, adrenaline appears to act as an endogenous agonist for tonically functioning presynaptic beta-adrenoceptors in renal arteries from prehypertensive young spontaneously hypertensive rats. Moreover, during and after a stressful situation, increased adrenaline appears to participate in further augmentation of vascular noradrenergic neurotransmission via further activation of these adrenoceptors to facilitate the release of noradrenaline.

Animals↗
PubMedDate not supplied

Release of [3H]- and endogenous GABA from slices of the rat medulla oblongata: modification by 3-mercaptopropionic acid, nipecotic acid and diaminobutyric acid.

Slices of the rat medulla oblongata were superfused and electrically stimulated. The amount of [3H]- and endogenous GABA was determined. There was a stimulus-evoked release of [3H]- and endogenous GABA, which was Ca2+-dependent and tetrodotoxin-sensitive. 3-Mercaptopropionic acid (3-MP) reduced the release of endogenous GABA, whereas the release of [3H]-GABA was not affected by this agent. Nipecotic acid enhanced the spontaneous and stimulus-evoked release of both [3H]- and endogenous GABA. 3-MP, nipecotic acid and diaminobutyric acid modified the stimulus-evoked release of endogenous GABA from slices containing the rostral ventrolateral medulla, the caudal ventrolateral medulla or the nucleus tractus solitarii, regions responsible for blood pressure regulation. These results suggest that 3-MP inhibits the stimulus-evoked release of GABA without affecting its release process, whereas nipecotic acid enhances the release via its uptake inhibition action.

3-Mercaptopropionic Acid↗