Abstract：
OBJECTIVE:To evaluate the consequence of pharmacologic inhibition of voltage-gated Na(+) channels (Nav) in the conscious rat, based on Nav having been implicated as modulators of rodent urodynamics using knockout as well as antisense oligodeoxynucleotide approaches. METHODS:The urodynamic response to standard Nav blockers, lamotrigine, amitriptyline, mexiletine, and carbamazepine were evaluated using conscious, continuous-filling cystometry in spontaneously hypertensive rats (SHRs). As a selectivity evaluation, the activity of the Nav blockers at muscarinic receptors was assessed via effect on carbachol-evoked bladder contractions. RESULTS:Lamotrigine, amitriptyline, mexiletine, and carbamazepine decreased peak micturition pressure, micturition interval, and void volume. These effects were markedly similar to observations with muscarinic antagonists. Therefore, we evaluated the selectivity of these agents against bladder muscarinic receptors. Lamotrigine, mexiletine, and carbamazepine had no effect on muscarinic bladder contractions, whereas amitriptyline displayed a robust antagonism of carbachol-induced contractility. CONCLUSION:Three Nav blockers--lamotrigine, mexiletine, and carbamazepine--demonstrated a reduction in micturition pressure and functional bladder capacity, similar to previous observations with muscarinic antagonists. These 3 Nav blockers are free of muscarinic antagonism, consistent with their cystometric effects being mediated via their Nav blocking activities. The negative findings reported here with Nav blockers suggest that Nav channel blockade is unlikely to reflect an improved treatment strategy for bladder disorders over currently prescribed muscarinic antagonists.
journal_name
Urologyjournal_title
Urologyauthors
Clouse AK,Jugus MJ,Eisennagel SH,Laping NJ,Westfall TD,Thorneloe KSdoi
10.1016/j.urology.2012.02.016subject
Has Abstractpub_date
2012-06-01 00:00:00pages
1410.e1-6issue
6eissn
0090-4295issn
1527-9995pii
S0090-4295(12)00182-3journal_volume
79pub_type
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