A comparison of pre- and postsynaptic effects of α-adrenolytic drugs in the pulmonary artery of the rabbit

1The potassium-evoked release of [3H]-noradrenaline from slices of rat occipital cortex and the potassium-evoked release of [3H]-5-hydroxytryptamine from slices of rat frontal cortex were measured using a superfusion system. 2 The rank order of potency for a number of a-adrenoceptor agonists was different for the two neuronal systems, clonidine and azepexole being the most potent inhibitors of noradrenaline release and methoxamine and phenylephrine being the most potent against 5-hydroxytryptamine release. 3 The rank order of potency for a series of a-adrenoceptor antagonists in reversing the inhibition of noradrenaline release produced by clonidine was: phentolamine > rauwolscine = yohimbine = corynanthine >> WB4101, whereas against methoxamine-inhibition of 5-hydroxytryptamine release the rank order of potency was: WB4101 > phentolamine > corynanthine > yohimbine > rauwolscine. 4 The results suggest that the a-adrenoceptors which modulate potassium-evoked 5-hydroxytryptamine release are not identical with the a2-adrenoceptors located on noradrenergic nerve terminals and may more closely resemble a,-than a2-adrenoceptors.

Section: Discussionmentioning

confidence: 82%

Different α‐adrenoceptors modulate the release of 5‐hydroxytryptamine and noradrenaline in rat cortex

Ennis

1983

“…At the end of experiments, tissues were solubilized in 2 ml of tissue solubilizer and the radioactivity in superfusate samples and tissues was determined by liquid scintillation counting. The basal outflow of tritium and the stimulation-evoked overflow of tritium were expressed as a percentage of the O The Macmillan Press Ltd 1985 tritium content of the tissue at the start of the respective stimulation period (see Borowski et al, 1977).…”

Section: Methodsmentioning

confidence: 99%

Evidence for neuro‐effector transmission through postjunctional α₂‐adrenoceptors in human saphenous vein

Docherty

Hyland

1985

1The effects of the ax-adrenoceptor antagonist prazosin and the x2-adrenoceptor antagonist yohimbine were examined against stimulation-evoked contractions in human isolated saphenous veins.2 The concentration of yohimbine producing 30% inhibition of stimulation-evoked contractions (IC30) was 13.2 nM, whereas the IC30 of prazosin was greater than 250 nM. 3 The inhibition of stimulation-evoked contractions by yohimbine was not prejunctionally mediated since yohimbine (0.01-0. I IM) significantly potentiated the stimulation-evoked overflow of tritium in tissues pre-incubated with [3H]-noradrenaline. 4 The high potency of yohimbine and the low potency of prazosin indicate that neuro-effector transmission in human saphenous vein is mediated predominantly by postjunctional M2-adrenoceptors.

“…Since phentolamine exhibits both al-and E2-adrenoceptor blocking activity (Borowski et al, 1977), it does not discriminate between a-adrenoceptor subtypes. Therefore, the contractile response to noradrenaline was investigated in the presence of yohimbine or prazosin.…”

Section: Adrenoceptor Subtypementioning

confidence: 99%

α₂‐Adrenoceptor‐mediated contractile response to catecholamines in smooth muscle strips isolated from rainbow trout stomach (Salmo gairdneri)

Kitazawa

Kondo

Temma

1986

1The type of adrenoceptor involved in the contractile response to catecholamines in smooth muscle strips isolated from rainbow trout stomach was determined.2 Noradrenaline (10 nM-10 ptM) and adrenaline (10 nM-3 pM) caused non-sustained contractions which were markedly decreased by phentolamine (5.4 pM) but not by carteolol (5 PM). Phenylephrine(1 jiM -1 mM) was less effective in causing muscle contraction and methoxamine produced no contraction. Clonidine (100 nM-300JM) caused no mechanical response but inhibited the contraction to noradrenaline or adrenaline but not acetylcholine or 5-hydroxytryptamine. 3 Yohimbine (10nM-1 pM) decreased the contraction induced by noradrenaline or adrenaline but prazosin (1 piM) did not. 4 Tetrodotoxin (780 nM) partially reduced the contraction induced by noradrenaline or adrenaline but atropine (500 nM) did not. 5 In the presence of atropine (1 pM), electrical transmural stimulation caused frequency-dependent, tetrodotoxin-sensitive contractions. 6 These results suggest that the contractile response induced by noradrenaline or adrenaline is mediated by M2-adrenoceptors. It is also suggested that noradrenaline and adrenaline contract the smooth muscle by direct action and by indirect action through the non-cholinergic excitatory nerve.