Atropine Resistance of Transmurally Stimulated Isolated Human Bladder Muscle

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Abstract
Human detrusor strips were obtained from patients undergoing reimplantation of ureters because of reflux, transvesical prostatectomy, or cysto-urethrectomy en bloc because of bladder malignancy. The strips were electrically stimulated. A frequency-dependent contractant response was obtained that was potentiated by physostigmine and abolished by tetrodotoxin. The maximum response approximately equaled that of acetylcholine in a maximum concentration. In most bladder preparations from patients without known functional bladder disturbances, atropine (0.01-0.1 .mu.M) had a marked inhibitory effect, and at concentrations exceeding 1 .mu.M the blockade was complete. In strips obtained from patients undergoing transvesical prostatectomy and who also had a cystometrically verified unstable bladder, there was a varying degree of atropine resistance with some preparations showing a 50% resistance to atropine. Prazosin, phentolamine, yohimbine, guanethidine, clonidine and noradrenaline [norepinephrine] had no consistent effects on the electrically induced bladder contraction. Nifedipine and nimodipine caused a maximum of 65% inhibition of the response. Addition of nimodipine to atropine-resistant strips when maximum atropine inhibition was reached abolished the contractions. Omitting Ca from the bath solution rapidly abolished the electrically induced contraction. In the normal human bladder, the contraction induced by electrical stimulation is mainly atropine sensitive. In the functionally disturbed bladder, part of the bladder contraction is atropine resistant, a finding that may have clinical implications.