Pharmacological action of nicotine in the isolated urinary bladder from rabbit: Special reference to the chronic nicotine treatment

Kizawa, Yasuo; Takayanagi, Issei; Shinkai, Michiko; Ohno, Yoshiko

doi:10.1016/0306-3623(88)90074-2

Cited by 9 publications

(9 citation statements)

References 19 publications

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“…Decreased sensitivity of peripheral adrenergic neurones and diminished responsiveness of detrusor muscle to nicotine have also been noted, respectively, in rats and rabbits receiving nicotine chronically (Haiggendal & Henning, 1980;Kizawa et al, 1988). The latter authors suggested that chronic nicotine treatment might cause a decrease in the number of nicotinic receptors and/or receptors for mediators released by nicotine .…”

Section: Discussionmentioning

confidence: 94%

“…(5) (5) (5) (Takayanagi et al, 1984;Kizawa & Takayanagi, 1985a,b;Kizawa et al, 1988;Takayanagi et al, 1988). The nicotine-induced contraction was potentiated by physostigmine and reduced greatly, but not completely, by atropine, suggesting that the main part of the contraction was due to release of acetylcholine from parasympathetic nerve terminals.…”

Section: Discussionmentioning

confidence: 99%

“…In chronic nicotine treatment, rabbits (initial body weight 2.7 + 0.1 kg, n = 14) drank either ordinary tap water or nicotine, 100mg (as a base) 1-1, for 4 weeks (Yamanaka et al, 1985;Kizawa et al, 1988 They were stored at -30°C.…”

Section: Methodsmentioning

confidence: 99%

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Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit

Hisayama

Shinkai

Takayanagi

et al. 1988

British J Pharmacology

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1 Nicotine produced a transient contraction of rabbit isolated iris sphincter muscle, a parasympathetic ganglion-free tissue. The response to nicotine was antagonized by hexamethonium, but was insensitive to tetrodotoxin (TTX). While single treatments with atropine, capsaicin or [D-Arg', D-Pro2, D-Trp7 9, Leu' ]-substance P (rpwwL-SP) partially blocked the response, combined treatment abolished it. 2 Chronic treatment of animals with nicotine added to the drinking water (about 12mg kg' per day) had no effect on the responsiveness to nicotine or the pharmacological properties of nicotineinduced contraction. 3 These results suggest that acetylcholine and tachykinin(s) released via sodium channelindependent mechanisms from nerve terminals of parasympathetic and primary sensory nerves, respectively, are involved in the nicotine-induced contractile response.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit

Hisayama

Shinkai

Takayanagi

et al. 1988

British J Pharmacology

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“…Nicotine has been reported to induce a tetrodotoxin rabbit and guinea-pig aorta (Ikushima et al, 1981; (TTX)-resistant response in many peripheral organs. 1982), nicotine has been considered to act on presyIn isolated preparations innervated by sympathetic naptic nicotinic receptors (Trendelenburg, 1965;Su nerves, such as rabbit pulmonary artery (Su & 1984;Kizawa et al, 1988;. It has also been reported that nicotine releases tachykinin(s) from chemosensitive sensory nerve in guinea-pig bronchus (Kizawa & Takayanagi, 1985) and rabbit iris sphincter (Hisayama et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of action of nicotine in isolated urinary bladder of guinea‐pig

Hisayama

Shinkai

Takayanagi

et al. 1988

British J Pharmacology

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1 Nicotine produced a transient contraction of isolated strips of guinea-pig urinary bladder. The response to nicotine was antagonized by the nicotinic receptor antagonist, hexamethonium but was insensitive to tetrodotoxin.2 The nicotine-induced contraction was potentiated by the cholinesterase inhibitor, physostigmine, and was reduced to 50% and 70% by the muscarinic cholinoceptor antagonist, atropine and the sympathetic neurone blocking drug, guanethidine, respectively. Chemical denervation with 6-hydroxydopamine abolished the inhibitory effect of guanethidine. Simultaneous treatment with atropine and guanethidine did not abolish the response to nicotine, but the degree of inhibition was comparable to that obtained with atropine alone.3 The nicotine-induced contraction was insensitive to bunazosin and yohimbine (al-and Cc2-adrenoceptor antagonists, respectively), and exogenously applied noradrenaline did not cause a contraction even in the presence of blockade of noradrenaline uptake mechanisms with desipramine and normetanephrine and of fi-adrenoceptors with propranolol, suggesting a non-adrenergic nature of the sympathomimetic effect of nicotine in this tissue. 4 The nicotine-induced contraction in the presence of atropine was abolished after desensitization of P2-purinoceptors with a, ,B-methylene adenosine 5'-triphosphate, a slowly degradable ATP analogue selective for P2-purinoceptors. By this desensitization, the response to ATP, but not to histamine, was also abolished.5 A cyclo-oxygenase inhibitor flurbiprofen partially inhibited the nicotine-induced contraction. The degree of the inhibition was more pronounced in the presence of atropine than in its absence. Flurbiprofen antagonized the response to exogenously applied ATP in an unsurmountable manner, but not that to carbachol.6 The present results suggest that nicotine might induce a contraction through an interaction with nicotinic receptors located on the terminals of, possibly, (i) parasympathetic cholinergic, (ii) sympathetic non-adrenergic and (iii) non-sympathetic purinergic nerves in guinea-pig detrusor preparations, and that a portion of the contraction due to the purine nucleotide released is possibly potentiated by intramural prostaglandin(s). Parasympathetic cholinergic output might be modulated by an unknown excitatory substance released by nicotine from sympathetic nerve.7 Nicotine reveals a latent excitatory effect of the sympathetic hypogastric nerve which innervates guinea-pig detrusor.

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“…Effects of Acetylcholine, Nicotine, Histamine, and EAS and antagonism on the guinea-pig ileum revealed that activity of EAS could be mediated by nicotinic receptor as extent of inhibition of Nicotine by Hexamethonium was comparable to EAS inhibition by Hexamethonium. Studies by Kizawa et al, (1988) 28 on a different the rabbit bladder suggests nicotine causing contraction on the bladder which was blocked by hexamethonium, atropine and capsaicin. This gives the indication that contractile responses on the bladder by nicotine may involve nicotine-induced responses and partly due to acetylcholine and tachykinnin release.…”

Section: Discussionmentioning

confidence: 99%

Preliminary pharmacological investigation of the ischuretic property and safety of a hydro-ethanolic extract of Amaranthus spinosis (Fam: Amaranthaceae)

Koffuor

Ainooson

Addotey

et al. 2013

Int J Basic Clin Pharmacol

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Background: Ischuria is a health and social problem, having a negative impact on sufferers. This study therefore was a preliminary investigation of the ischuretic property and safety for use of a hydro-ethanolic extract of Amaranthus spinosus used traditionally in managing ischuria. Methods: Phytochemical screening, thin layer chromatography and high performance liquid chromatography were performed on the extract to establish fingerprints for identification. Acetylcholine, Nicotine, and the extract were applied to an isolated rat urinary bladder to ascertain contractile response. The possible receptor site(s) of action was also investigated using isolated rabbit jejunum, and guinea-pig ileum preparations. In-house observation, hematological analysis, and liver and kidney function tests were performed on Sprague-Dawley rats, in acute and sub-acute toxicity studies. Results: The extract had contractile effects on the rat urinary bladder (similar to acetylcholine and nicotine) and rabbit jejunum. Its contractile effect of the guinea-pig ileum was significantly inhibited by hexamethonium (77.50 ± 8.50 %; P ≤ 0.001) and to a lesser extent by mepyramine (49.2 ± 6.80 %; P ≤ 0.001) and Atropine (22.45 ± 5.22 %; P ≤ 0.01). The extract (80-800 mg kg-1) was not lethal and a 160 and 240 mg kg-1 dose had no adverse effect on blood, liver, kidney metabolic function. Conclusions: The hydro-ethanolic extract of Amaranthus spinosus has ischuretic activity possibly mediated via nicotinic, histaminic and muscarinic receptor stimulation and is safety to use in ischuria. [Int J Basic Clin Pharmacol 2013; 2(5.000): 517-527

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Pharmacological action of nicotine in the isolated urinary bladder from rabbit: Special reference to the chronic nicotine treatment

Cited by 9 publications

References 19 publications

Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit

Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit

Mechanism of action of nicotine in isolated urinary bladder of guinea‐pig

Preliminary pharmacological investigation of the ischuretic property and safety of a hydro-ethanolic extract of Amaranthus spinosis (Fam: Amaranthaceae)

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