The Effect of Prazosin on the Guinea‐pig Ileum

Fagbemi, Shamusi; Salako, L.A.

doi:10.1111/j.1476-5381.1980.tb08715.x

Cited by 13 publications

(9 citation statements)

References 12 publications

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“…This action is mediated via a2-adrenoceptors as it is blocked by the selective a2-adrenoceptor antagonist, rauwolscine (Weitzell et al, 1979;Timmermans et al, 1980) but not by the a,-adrenoceptor antagonist, prazosin (Davey, 1980). Both agents were used in concentrations selective for al-and a2-adrenoceptors respectively in other tissues (Tanaka et al, 1978;Fagbemi & Salako, 1980). Our previous observation that 10-M clonidine did not influence the NANC relaxation by electrical stimulation at 5 Hz during 45 s might be due to the partial agonism and limited selectivity of this agent for a2-adrenoceptors.…”

Section: Resultsmentioning

confidence: 99%

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304

Lefebvre

Smits

1992

British J Pharmacology

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1 The influence of the X2-adrenoceptor agonist, UK-14,304, on non-adrenergic non-cholinergic (NANC) relaxation induced by electrical field stimulation was investigated in longitudinal muscle strips of the gastric fundus of reserpinized rats.2 In tissues where tone was raised by 3 x l0' M prostaglandin F2, (PGF2.), the inhibitory effect of 10-6 M UK-14,304, on the NANC relaxations induced by short train stimulation (40 V, I ms, 20 s) was inversely related to the stimulus frequency (1-4-16 Hz). UK-14,304 (10-6 M) did not influence relaxations induced by administration of exogenous nitric oxide (NO, 2 x 10-6 M-10-4 M). The inhibitory effect of UK-14,304 on the electrically induced relaxations was antagonized by 10-6 M rauwolscine but not by 10-6 M prazosin. 3 UK-14,304 (10-6 M) also reduced the amplitude of the sustained NANC relaxation, induced by electrical field stimulation (40 V, 1 ms, 4 Hz) for 5 min. The effect of UK-14,304 was also antagonized by 10-6 M rauwolscine but not by 10-6 M prazosin. UK-14,304 (10-6 M) did not reduce the relaxation induced by 3 x 10-M vasoactive intestinal polypeptide (VIP). 4 These results suggest that the release of the inhibitory NANC neurotransmitter during short train stimulation, thought to be NO, and during sustained stimulation, thought to be VIP, is inhibited by stimulation of presynaptic x2-adrenoceptors in the rat gastric fundus.

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Section: Resultsmentioning

confidence: 99%

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304

Lefebvre

Smits

1992

British J Pharmacology

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“…These results demonstrate the presence of postsynaptic inhibitory M and P-adrenoceptors in the longitudinal muscle of the mouse colon. These receptors have been described in various gastrointestinal preparations including the guinea-pig isolated ileum (Wikberg, 1977;Fagbemi & Salako, 1980), the rabbit intestine (Bowman & Hall, 1970;Wikberg, 1977), the mouse ileum (Large & Wright, 1974). In conclusion, in the mouse colon, the activation of prejunctional M2-adrenoceptors leads to a contraction.…”

Section: Postsynaptic Adrenoceptorsmentioning

confidence: 94%

Adrenoceptors and regulation of intestinal tone in the isolated colon of the mouse

Fontaine¹,

Grivegnee²,

Reuse³

1984

British J Pharmacology

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1 Adrenaline, noradrenaline, phenylephrine, dopamine, clonidine and apomorphine at low concentrations (from 10 9M to 10-6 M) contracted the longitudinal muscle of the isolated distal colon of the mouse. Phentolamine, tetrodotoxin and indomethacin antagonized these contractile responses. Yohimbine antagonized them at lower concentrations than prazosin. Dopamine and clonidine had the same contractile activity on preparations from mice pretreated with 6-hydroxydopamine (6-OHDA). Isoprenaline (10-9 to 3 x 10-7M) induced relaxations of the colon which were antagonized by propranolol.2 At higher concentrations, adrenaline and noradrenaline (from 3 x 10-7 M), dopamine (from 3 x 10 -5M), phenylephrine (from 3 x 10-6M) and apomorphine (from 10-4M) relaxed the colon.Clonidine (10-6 to 3 x 10-5 M) inhibited the spontaneous activity of the colon but never induced relaxations. At 10-4 and 10-3 M clonidine elicited contractions. Prazosin antagonized the inhibitory effect of phenylephrine and clonidine, a mixture of propranolol and prazosin antagonized the relaxations to adrenaline, noradrenaline and dopamine and unmasked contractions that were sensitive to yohimbine and tetrodotoxin. The relaxations induced by apomorphine and the contractions induced by clonidine (> 10-6 M) were resistant to all these antagonists. 3 Electrical field stimulation (1ms, 2 Hz, 2-20 V) of the mouse colon induced contractile responses which increased with the frequency of the stimulus. After cessation of stimulation at 4 Hz a rebound contraction was generally observed, followed by a progressive decline in tone. In the presence of atropine, the contractile response to field stimulation was abolished and transformed into a rapid and sustained relaxation. A rebound contraction was always observed after cessation of stimulation. The responses to electrical stimulation (in the presence or absence of atropine) were abolished by tetrodotoxin. The rebound contractions were abolished by indomethacin. The relaxations induced in the presence of atropine were not modified by phentolamine, propranolol, guanethidine, methysergide, mepyramine, cimetidine or naloxone.4 Tetrodotoxin (from 3 x 10-8 M) caused a sustained contraction of the colon with increased spontaneous activity. This contraction was not modified by atropine, phentolamine, propranolol, guanethidine, methysergide, mepyramine, cimetidine, naloxone, but was abolished by preincubation of the preparation with indomethacin. 5 These results indicate that, at low concentrations, various sympathomimetics contracted the mou.e distal colon by stimulating M2 presynaptic adrenoceptors. The responses appeared provided intramural prostaglandin synthesis was unaffected. Higher concentrations of sympathomimetics induced relaxations by stimulation of postjunctional a1-and 3-adrenoceptors. Electrical field stimulation of the mouse colon produced cholinergically mediated contractions or, in the presence of atropine, non-adrenergic non-cholinergic (NANC) relaxations followed by rebound contractions, provided prostaglan...

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“…In the isolated guinea-pig ileum, a2-adrenoceptor agonists inhibit acetylcholine release, resulting in a reduction of the amplitude of electrically evoked contractions, and these inhibitions are antagonized by yohimbine (Kilbinger & Wessler, 1979;Andrejak, Pommier, Mouille' & Schmitt, 1980;Fagbemi & Salako, 1980). Yohimbine also antagonizes the inhibition of field-stimulated contractions induced by peri-arterial nerve stimulation (Fagbemi & Salako, 1980).…”

Section: Intestinal Inhibitory Reflex By Capsaicin Discussionmentioning

confidence: 99%

Capsaicin‐sensitive afferents activate a sympathetic intestinointestinal inhibitory reflex in dogs.

Mizutani

Neya

Nakayama

1990

The Journal of Physiology

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SUMMARY1. In urethane-anaesthetized dogs, an intra-arterial infusion of capsaicin (0-7-14 nmol min-) into a separated jejunal segment inhibited a vagally evoked cholinergic contraction of the other non-infused segments. The mechanism of this reflex was investigated.2. The inhibition by capsaicin was abolished after bilateral splanchnic nerve section or cervical spinal cord transaction (C5 or C6), but was unaffected by bilateral vagotomy. Decerebration partially reduced the inhibition.3. The inhibition by capsaicin was abolished by pre-treatment with phentolamine or yohimbine, but was unaffected by prazosin or propranolol.4. Sympathetic efferent discharge of the mesenteric nerve increased with capsaicin application, during which time vagally evoked contractions were inhibited.5. Single-unit discharges of the major splanchnic and mesenteric afferents increased with capsaicin infusion to the loop which was innervated by the units.6. Together the results implied that capsaicin stimulated canine intestinal primary afferents, resulting in the sympathetic intestinointestinal inhibitory reflex supraspinally. The inhibition of vagally evoked contractions may be due to a presynaptic inhibition via a2-adrenoceptors, which are activated by the reflex.

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The Effect of Prazosin on the Guinea‐pig Ileum

Cited by 13 publications

References 12 publications

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304

Adrenoceptors and regulation of intestinal tone in the isolated colon of the mouse

Capsaicin‐sensitive afferents activate a sympathetic intestinointestinal inhibitory reflex in dogs.

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The Effect of Prazosin on the Guinea‐pig Ileum

Cited by 13 publications

References 12 publications

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α2‐adrenoceptor agonist, UK‐14,304

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α2‐adrenoceptor agonist, UK‐14,304

Adrenoceptors and regulation of intestinal tone in the isolated colon of the mouse

Capsaicin‐sensitive afferents activate a sympathetic intestinointestinal inhibitory reflex in dogs.

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Product

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Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304

Modulation of non‐adrenergic non‐cholinergic inhibitory neurotransmission in rat gastric fundus by the α₂‐adrenoceptor agonist, UK‐14,304