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Angiotensin Receptor Blocker Losartan Inhibits Spontaneous Motility of Isolated Human Ureter

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Abstract

Background and Objectives

Ureteral motility is essential for elimination of intraluminal stones, and it may be adversely affected by cardiovascular drugs that a patient is taking chronically. The aim of our study was to test whether ACE inhibitors and an angiotensin receptor blocker may influence spontaneous contractions of isolated human ureter.

Methods

Both phasic and tonic contractions of the isolated ureteral segments taken from 10 patients were measured as changes of the longitudinal tension or pressure recordings. Captopril, enalapril and losartan were separately added to the organ baths cumulatively.

Results

While enalapril (2.7 × 10−7–3.9 × 10−4 M) and captopril (6.1 × 10−7–2.7 × 10−3 M) did not affect either spontaneous activity or tone of isolated ureteral segments, losartan (2.9 × 10−7–4.2 × 10−4 M) caused concentration-dependent inhibition of spontaneous contractions of the segments (50 % effective concentration (EC50) = 13.46 ± 1.80 × 10−6 M; F = 10.72, r = 0.79, p < 0.001).

Conclusions

Due to differences in molecular mechanism of action, angiotensin receptor blocker losartan does and ACE inhibitors captopril and enalapril do not inhibit spontaneous contractions of isolated human ureter.

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Correspondence to Slobodan M. Jankovic.

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Funding

The work described in this article was partially financed by Grant No. 175007 given by Serbian Ministry of Education, and by Grant No. 404 given by Ministry of Science of Montenegro.

Conflict of interest

The authors of this article do not have any conflict of interest in relation to its contents.

Ethical approval

All procedures in this study were in accordance with the 1964 Helsinki declaration (and its amendments), and the Ethical Committee of Clinical Center Kragujevac, Serbia, approved the study.

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Jankovic, S.M., Stojadinovic, D., Stojadinovic, M. et al. Angiotensin Receptor Blocker Losartan Inhibits Spontaneous Motility of Isolated Human Ureter. Eur J Drug Metab Pharmacokinet 41, 835–838 (2016). https://doi.org/10.1007/s13318-015-0298-x

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  • DOI: https://doi.org/10.1007/s13318-015-0298-x

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