Potential therapeutic targets for the treatment of detrusor overactivity

Russell Chess-William

Research output: Contribution to journalReview articleResearchpeer-review

22 Citations (Scopus)

Abstract

Current treatments for the overactive detrusor are poorly tolerated and can exert significant adverse effects. Possible targets for the development of new treatments are considered. Potential targets in four locations are examined: detrusor smooth muscle, urothelium, peripheral nerves and the CNS. In the detrusor, the role of various muscarinic receptor subtypes is discussed and β-adrenoceptor agonists, phosphodiesterase inhibitors and potassium channel openers, all of which inhibit detrusor contractility, are considered for drug development. in the urothelium, a number of substances are released that affect bladder function including ATP, acetylcholine and an inhibitory factor that has yet to be identified. All three systems have the potential to be novel targets for drug development. Other possible therapeutic targets are the mechanisms influencing transmitter release in the bladder, for example, prejunctional 5-hydroxytryptamine (5-HT 4 receptors. Finally, targets within the CNS and spinal cord are considered, including opioid receptors, 5-HT receptors and α-adrenoceptors. 2004

Original languageEnglish
Pages (from-to)95-106
Number of pages12
JournalExpert Opinion on Therapeutic Targets
Volume8
Issue number2
DOIs
Publication statusPublished - Apr 2004
Externally publishedYes

Fingerprint

Urothelium
Serotonin Receptors
Adrenergic Receptors
Serotonin
Urinary Bladder
Overactive Urinary Bladder
Phosphodiesterase Inhibitors
Potassium Channels
Opioid Receptors
Muscarinic Receptors
Peripheral Nerves
Pharmaceutical Preparations
Acetylcholine
Smooth Muscle
Muscle
Transmitters
Spinal Cord
Adenosine Triphosphate
Therapeutics

Cite this

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Potential therapeutic targets for the treatment of detrusor overactivity. / Chess-William, Russell.

In: Expert Opinion on Therapeutic Targets, Vol. 8, No. 2, 04.2004, p. 95-106.

Research output: Contribution to journalReview articleResearchpeer-review

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