Characterization of .ALPHA.-adrenoceptor subtypes involved in regulation of ureteral fluid transport.

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Abstract
Experiments were carried out in the dog by the use of experimental procedure which permits to assess independently changes in uretheral peristaltic frequency, bolus volume and intraluminal pressure and flow volume in order to characterize .alpha.-adrenoceptor subtypes involved in regulation or ureteral urine transport. Norepinephrine caused an increase in ureteral peristaltic frequency, an elevation in intraureteral baseline and contractile pressure and a decrease in bolus volume, with a resultant decrease in the rate of fluid transport. Phenylephrine (.alpha.1-agonist) and clonidine (.alpha.2-agonist) caused the effects similar to those of norepinephrine on peristaltic frequency, intraureteral baseline and contractile pressure, and bolus volume. Phentolamine (non-selective .alpha.-antagonist) and prazosin (.alpha.1-antagonist) caused a decrease in ureteral peristaltic frequency, and a fall in intraureteral baseline and contractile pressure, and yohimbine (.alpha.2-antagonist) abolished peristalsis and bolus formation. These changes were accompanied by an increase in the rate of fluid transport. These data suggest that the ureteral urine transport is controlled by activation of both .alpha.1- and .alpha.2-adrenoceptors through regulation of peristaltic frequency and bolus volume.