Physiologic Effect of Nifedipine and Tamsulosin on Contractility of Distal Ureter

Abstract

Renal colic not only leads to significant morbidity but imposes a financial burden on society in lost productivity and healthcare dollars spent. Both tamsulosin and nifedipine can facilitate spontaneous stone passage in the distal ureter and reduce the associated colic. We evaluated the physiologic effect of these agents on the distal pig ureter. Bilateral ureters were removed en bloc with the bladder trigone from three pigs. Five-millimeter rings were taken from the intramural and distal ureter. Isometric tension recording was performed during both spontaneous and electrically stimulated contraction. Measurements of contractile interval and amplitude were taken in baseline buffer solution, nifedipine at 10(-6) g/L, and tamsulosin at 10(-6) g/L. Spontaneous contractile activity was also measured with phenylephrine at 10(-4) g/L followed by tamsulosin at 10(-6) g/L. Under conditions of spontaneous contractility, phenylephrine decreased the contraction interval by 46%, an effect which was reversed by tamsulosin. Tamsulosin increased the baseline interval by 27% (P < 0.025) and decreased the amplitude by 7% (P > 0.1). Nifedipine blocked all contractile activity. Under stimulated contractility, tamsulosin had no effect on the interval and decreased the amplitude by 7% (P > 0.1). Nifedipine blocked all contractile activity. We believe that both tamsulosin and nifedipine prevent the disorganized antiperistalsis associated with ureteral spasm while allowing some degree of antegrade fluid-bolus (stone) propagation. It is this mechanism of action that facilitates spontaneous passage and reduces associated renal colic when tamsulosin and nifedipine are used for the management of ureteral stone disease.