Motor responses of the urinary bladder and skeletal muscle in <i>Botulinum</i> intoxicated rats

Carpenter, F. G.

doi:10.1113/jphysiol.1967.sp008119

Cited by 58 publications

(26 citation statements)

References 12 publications

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“…botulinum toxin (Carpenter, 1967). This study is concerned with the action of ecothiophate and atropine on nerve-induced responses of the urinary bladder in vitro.…”

Section: Introductionmentioning

confidence: 99%

Atropine Resistance and Muscarinic Receptors in the Rat Urinary Bladder

Carpenter

1977

British J Pharmacology

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1The action of an anticholinesterase and an antimuscarinic drug upon nerve-induced contractions of the rat urinary bladder were examined during transmural stimulation at 20 Hz. Responses were graded in magnitude by limiting the duration of the stimulus trains. 2 Responses of low magnitude produced by short stimulus trains were unchanged by atropine; however, maximal responses resulting from long stimulus trains were diminished in magnitude and shortened in duration. 3 Responses of small magnitude elicited by short stimulus trains involve muscarinic receptors in close proximity to the neuroeffector junction and are resistant to atropine. 4 Maximal responses elicited by long stimulus trains involve'junctional' muscarinic receptors as well as receptors located at the periphery of the junction; the 'extrajunctional' receptors are blocked by atropine. 5Responses of low magnitude produced by short stimulus trains were unaffected by echothiophate; however, the duration of maximal responses resulting from the long stimulus trains was extended. 6 The inhibition of cholinesterase did not increase the occupation of muscarinic receptors by the transmitter; however, after large quantities of transmitter were released by the long stimulus trains the association between the receptors and acetylcholine was prolonged.

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“…botulinum toxin (Carpenter, 1967). This study is concerned with the action of ecothiophate and atropine on nerve-induced responses of the urinary bladder in vitro.…”

Section: Introductionmentioning

confidence: 99%

Atropine Resistance and Muscarinic Receptors in the Rat Urinary Bladder

Carpenter

1977

British J Pharmacology

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“…Type A Clostridium botulinum toxin was administered as an acetate buffered solution containing 2 mg of the crystalline protein. Doses 100 to 1000 times larger than the LD were administered intraperitoneally to the rats to reduce the time required for the onset of symptoms to 4 to 6 h; 1000 x LD of type A toxin was found to produce terminal symptoms of botulism within 3 to 5 h (Carpenter, 1967).…”

Section: Methodsmentioning

confidence: 99%

“…The single stimulus responses are not abolished by high concentrations of atropine (10-5 M) while the responses to a maximal dose of a cholinomimetic drug are abolished by only 5 x lo-7 M atropine. A further difference between the two types of response is related to the magnitude; at the optimal stimulus rate the nerveinduced responses are 50% greater than those resulting from the cholinomimetic drug (Carpenter, 1967).…”

Section: Introductionmentioning

confidence: 99%

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Potentiation of Nerve‐induced Bladder Responses by Tetraethylammonium in Relation to Junctional and Extrajunctional Muscarinic Receptors

Carpenter

1978

British J Pharmacology

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IThe single stimulus responses elicited in the rat urinary bladder were enhanced up to 3 fold by tetraethylammonium chloride (TEA) 4 The responses of bladders to carbachol were dose-dependent in the range 10-6 to 10' M and were atropine-sensitive. After 5 mm TEA the means of the responses produced by graded doses of carbachol were less than control; muscarinic receptors that were blocked by TEA are probably also atropine-sensitive. 5 It is suggested that muscarinic receptors in the rat urinary bladder may be divided into: (1) junctional receptors that are resistant to atropine and may be indirectly affected by TEA and (2) extrajunctional receptors that are blocked by atropine and may be directly affected by TEA.

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“…[52][53][54] A marked loss of contraction in a rat bladder after acute botulinum poisoning with decrease in acetylcholine release at motor nerve stimulation was observed by Carpenter. 55 The effect of injecting botulinum-A toxin into the human detrusor muscle in patients with neurogenic detrusor overactivity was first reported in 2000 in a nonrandomised prospective study. 56,57 The patients with spinal cord injury selected for a preliminary study had severe neurogenic detrusor overactivity and suffered from incontinence resistant to anticholinergic drugs.…”

Section: Botulinum-a Toxin Injection Into the Detrusor Musclementioning

confidence: 99%

Intravesical therapy options for neurogenic detrusor overactivity

Reitz

Schurch

2004

Spinal Cord

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Objectives: This review considers intravesical treatment options of neurogenic detrusor overactivity and discusses the underlying mechanism of action, clinical safety and efficacy, and the future trends. Methods: The available literature was reviewed using medline services. Results: Oral anticholinergic drugs are widely used to treat detrusor overactivity, but they are ineffective in some patients or cause systemic side effects such as blurred vision or dry mouth. As an alternative, topical therapy strategies have been suggested to achieve a profound inhibition of the overactive detrusor and to avoid high systemic drug levels. Currently available intravesical treatment options either act on the afferent arc of the reflex such as local anaesthetics or vanilloids or on the efferent cholinergic transmission to the detrusor muscle such as intravesical oxybutynin or botulinum toxin. Although an established and effective therapy, intravesical oxybutynin is not widely used. Evidence for clinical significance of intravesical atropine and local anaesthetic is missing. Intravesical capsaicin has been shown to improve clinical and urodynamic parameters, but cause pain in some patients. The intravesical instillation of resiniferatoxin and the injection of botulinum-A toxin into the detrusor muscle are promising new options; however, randomised placebo-controlled studies to prove their safety and efficacy are still missing. Conclusion: Intravesical treatment strategies in patients with neurogenic detrusor overactivity may provide alternatives to established therapies such as oral anticholinergics. The selectivity of the intravesical treatment and the reduction or even the absence of side effects are major advantages of this topical approach.

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Motor responses of the urinary bladder and skeletal muscle in Botulinum intoxicated rats

Cited by 58 publications

References 12 publications

Atropine Resistance and Muscarinic Receptors in the Rat Urinary Bladder

Atropine Resistance and Muscarinic Receptors in the Rat Urinary Bladder

Potentiation of Nerve‐induced Bladder Responses by Tetraethylammonium in Relation to Junctional and Extrajunctional Muscarinic Receptors

Intravesical therapy options for neurogenic detrusor overactivity

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