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Prostaglandin-independent decrease of sheep ureter contractility induced by bradykinin
1Department of Physiology, Faculty of Medicine, University of Osmangazi, Eskişehir, Turkey.
Renal Physiology and Biochemistry
|January 1, 1995
Summary
Bradykinin significantly reduces ureteral contractility. This effect does not involve prostaglandins, as inhibiting their synthesis did not alter bradykinin's impact on ureteral smooth muscle function.
Area of Science:
- Urology
- Pharmacology
- Physiology
Background:
- Mechanisms of bradykinin action on ureteral motility are not well understood.
- The potential role of prostaglandins in mediating bradykinin's effects on the ureter has not been previously investigated.
Purpose of the Study:
- To investigate the effects of bradykinin on sheep ureteral contractility.
- To determine if prostaglandins mediate bradykinin-induced changes in ureteral motility.
Main Methods:
- Sheep ureteral strips were used to measure contractility.
- Bradykinin was applied at various concentrations (10(-8) to 10(-6) M).
- Prostaglandin synthesis was inhibited using indomethacin, sodium salicylate, and aspirin.
Main Results:
- Bradykinin caused significant reductions in ureteral contractile force.
- Inhibition of prostaglandin synthesis also decreased ureteral contractility.
- Even with inhibited prostaglandin synthesis, bradykinin still significantly reduced contractility.
Conclusions:
- Bradykinin decreases ureteral contractility through a mechanism independent of prostaglandin generation.
- Prostaglandins do not appear to mediate the effects of bradykinin on ureteral smooth muscle.