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The role of angiotensin II in stress urinary incontinence: A rat model.
Neurourol Urodyn. 2007; 26(1):81-8; discussion 89.NU

Abstract

AIMS

Pharmacological treatment for stress urinary incontinence (SUI) is limited to the use of non-selective alpha-agonists, which are often ineffective. Non-adrenergic mechanisms have also been implicated in urethral closure, including angiotensin II (Ang-II), which has been demonstrated throughout the urinary tract. We investigate the role of Ang-II in urethral tone in a rat model of SUI.

METHODS

Abdominal leak point pressure (ALPP) and retrograde urethral pressure profilometry (RLPP) were measured in 70 female virgin rats. Thirty rats underwent pudendal nerve injury (PNT), 30 had circumferential urethrolysis (U-Lys), and 10 had sham surgery. Rats received daily doses of Angiotensin Type 1 (AT-1) receptor inhibitor (20 mg/kg), Angiotensin Type 2 (AT-2) receptor antagonist (10 mg/kg), or Ang-II (2 mg/kg).

RESULTS

Following U-Lys, RLPP and ALPP decreased from 21.4 +/- 2.0 and 39.2 +/- 3.3 mm Hg, to 13.1 +/- 1.5 and 21.6 +/- 1.9 mmHg, respectively (P < 0.01). After PNT, RLPP, and ALPP decreased from 21.0 +/- 1.6 and 41.9 +/- 3.0 mmHg to 13.1 +/- 1.5 and 24.7 +/- 3.3 mmHg, respectively (P < 0.01). AT-1 inhibitor caused significant decrease in RLPP and ALPP from 21.0 +/- 6.2 and 41.8 +/- 9.4 mmHg, to 12.0 +/- 3.8 and 25.6 +/- 6.6 mmHg, respectively (P < 0.01). Likewise, AT-2 treatment reduced RLPP and ALPP from 21.4 +/- 6.3 and 40.1 +/- 1.7 mmHg, to 13.5 +/- 5.7 and 31.0 +/- 7.2 mmHg, respectively (P < 0.01). Following surgery, Ang-II administration restored RLPP and ALPP to baseline presurgical values.

CONCLUSIONS

AT-1 and AT-2 receptor inhibition significantly lowers urethral resistance, comparable to either neurogenic or urethrolytic injury. Ang-II treatment restored urethral tone in rats with intrinsic sphincter dysfunction. Ang II appears to serve a functional role in the maintenance of urethral tone and stress continence.

Authors+Show Affiliations

Section of Urology, Department of Surgery, University of Arizona Health Sciences Center, Tucson, Arizona, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17029249

Citation

Phull, Hardeep, et al. "The Role of Angiotensin II in Stress Urinary Incontinence: a Rat Model." Neurourology and Urodynamics, vol. 26, no. 1, 2007, pp. 81-8; discussion 89.
Phull H, Salkini M, Escobar C, et al. The role of angiotensin II in stress urinary incontinence: A rat model. Neurourol Urodyn. 2007;26(1):81-8; discussion 89.
Phull, H., Salkini, M., Escobar, C., Purves, T., & Comiter, C. V. (2007). The role of angiotensin II in stress urinary incontinence: A rat model. Neurourology and Urodynamics, 26(1), 81-8; discussion 89.
Phull H, et al. The Role of Angiotensin II in Stress Urinary Incontinence: a Rat Model. Neurourol Urodyn. 2007;26(1):81-8; discussion 89. PubMed PMID: 17029249.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of angiotensin II in stress urinary incontinence: A rat model. AU - Phull,Hardeep, AU - Salkini,Mohamad, AU - Escobar,Christina, AU - Purves,Todd, AU - Comiter,Craig V, PY - 2006/10/10/pubmed PY - 2007/3/28/medline PY - 2006/10/10/entrez SP - 81-8; discussion 89 JF - Neurourology and urodynamics JO - Neurourol Urodyn VL - 26 IS - 1 N2 - AIMS: Pharmacological treatment for stress urinary incontinence (SUI) is limited to the use of non-selective alpha-agonists, which are often ineffective. Non-adrenergic mechanisms have also been implicated in urethral closure, including angiotensin II (Ang-II), which has been demonstrated throughout the urinary tract. We investigate the role of Ang-II in urethral tone in a rat model of SUI. METHODS: Abdominal leak point pressure (ALPP) and retrograde urethral pressure profilometry (RLPP) were measured in 70 female virgin rats. Thirty rats underwent pudendal nerve injury (PNT), 30 had circumferential urethrolysis (U-Lys), and 10 had sham surgery. Rats received daily doses of Angiotensin Type 1 (AT-1) receptor inhibitor (20 mg/kg), Angiotensin Type 2 (AT-2) receptor antagonist (10 mg/kg), or Ang-II (2 mg/kg). RESULTS: Following U-Lys, RLPP and ALPP decreased from 21.4 +/- 2.0 and 39.2 +/- 3.3 mm Hg, to 13.1 +/- 1.5 and 21.6 +/- 1.9 mmHg, respectively (P < 0.01). After PNT, RLPP, and ALPP decreased from 21.0 +/- 1.6 and 41.9 +/- 3.0 mmHg to 13.1 +/- 1.5 and 24.7 +/- 3.3 mmHg, respectively (P < 0.01). AT-1 inhibitor caused significant decrease in RLPP and ALPP from 21.0 +/- 6.2 and 41.8 +/- 9.4 mmHg, to 12.0 +/- 3.8 and 25.6 +/- 6.6 mmHg, respectively (P < 0.01). Likewise, AT-2 treatment reduced RLPP and ALPP from 21.4 +/- 6.3 and 40.1 +/- 1.7 mmHg, to 13.5 +/- 5.7 and 31.0 +/- 7.2 mmHg, respectively (P < 0.01). Following surgery, Ang-II administration restored RLPP and ALPP to baseline presurgical values. CONCLUSIONS: AT-1 and AT-2 receptor inhibition significantly lowers urethral resistance, comparable to either neurogenic or urethrolytic injury. Ang-II treatment restored urethral tone in rats with intrinsic sphincter dysfunction. Ang II appears to serve a functional role in the maintenance of urethral tone and stress continence. SN - 0733-2467 UR - https://www.unboundmedicine.com/medline/citation/17029249/The_role_of_angiotensin_II_in_stress_urinary_incontinence:_A_rat_model_ L2 - https://doi.org/10.1002/nau.20339 DB - PRIME DP - Unbound Medicine ER -