The Effect of Angiotensin Converting Enzyme Inhibition and Angiotensin II Receptor Antagonism on Obstructed Rat Bladder

Palmer, Lane S.; Lee, Chung; Decker, Robert S.; Lang, Sharon; Kaplan, William E.; Firlit, Casimir F.; Cheng, Earl Y.

doi:10.1016/s0022-5347(01)64397-0

Cited by 17 publications

(21 citation statements)

References 28 publications

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“…Ang-II has also been shown to exist and function throughout the genitourinary system including the ureter [Santis et al, 2003], penis [Comiter et al, 1997a], and bladder [Cheng et al, 1999]. Detrusor strips have shown that angiotensin converting enzyme (ACE) locally converts Angiotensin I to Ang-II, which is then able to target nearby smooth muscle in a paracrine fashion by binding to AT-1 and -2 receptors [Palmer et al, 1997]. Subsequent activation of the AT-1 receptor, in particular, is responsible for mediating bladder smooth muscle contractions [Tanabe et al, 1993].…”

Section: Discussionmentioning

confidence: 99%

The role of angiotensin II in stress urinary incontinence: A rat model

Phull

Salkini

Escobar

et al. 2006

Neurourology and Urodynamics

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Aims: Pharmacological treatment for stress urinary incontinence (SUI) is limited to the use of nonselective alpha-agonists, which are often ine¡ective. 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 pro¢lome-try (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 AE 2.0 and 39.2 AE 3.3 mm Hg, to 13.1 AE1.5 and 21.6 AE 1.9 mmHg, respectively (P<0.01). After PNT, RLPP, and ALPP decreased from 21.0 AE 1.6 and 41.9 AE 3.0 mmHg to 13.1 AE1.5 and 24.7 AE 3.3 mmHg, respectively (P<0.01). AT-1 inhibitor caused signi¢cant decrease in RLPP and ALPP from 21.0 AE 6.2 and 41.8 AE 9.4 mmHg, to 12.0 AE 3.8 and 25.6 AE 6.6 mmHg, respectively (P<0.01). Likewise, AT-2 treatment reduced RLPP and ALPP from 21.4 AE 6.3 and 40.1 AE1.7 mmHg, to 13.5 AE 5.7 and 31.0 AE 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 signi¢cantly 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.

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Section: Discussionmentioning

confidence: 99%

The role of angiotensin II in stress urinary incontinence: A rat model

Phull

Salkini

Escobar

et al. 2006

Neurourology and Urodynamics

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“…Stretch-stimulated growth of rat bladder smooth muscle cells was shown to involve the ATII receptor system (Nguyen et al, 2000). On the other hand, inhibition of ACE or blockade of ATII receptors had no effect on the development of bladder hypertrophy in rats (Persson et al, 1996;Palmer et al, 1997).…”

Section: Peripheral Targetsmentioning

confidence: 98%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

452

364

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“…The effect of AT2 on bladder smooth muscle tone was minor but was mediated by stimulation of the AT1 subtype receptor. Palmer et al 132 arrived at a similar conclusion, showing that neither captopril nor losartan significantly ameliorated the histologic or biochemical features of partial BOO in the rat.…”

Section: Angiotensin Receptor Antagonistsmentioning

confidence: 82%

LUTS treatment: Future treatment options

2007

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Lower urinary tract symptoms (LUTS) are commonly divided into storage, voiding, and postmicturition symptoms, and may occur in both men and women. Male LUTS have historically been linked to benign prostatic hyperplasia (BPH), but are not necessarily prostate related. The focus of treatment for LUTS has thus shifted from the prostate to the bladder and other extraprostatic sites. LUTS include symptoms of the overactive bladder (OAB), which are often associated with detrusor overactivity. Treatment for LUTS suggestive of BPH has traditionally involved the use of alpha(1)-adrenoceptor (AR) antagonists; 5alpha-reductase inhibitors; and phytotherapy-however, several new therapeutic principles have shown promise. Selective beta(3)-adrenoceptor agonists and antimuscarinics are potentially useful agents for treating LUTS, particularly for storage symptoms secondary to outflow obstruction. Other agents of potential or actual importance are antagonists of P2X(3) receptors, botulinum toxin type A, endothelin (ET)-converting enzyme inhibitors, and drugs acting at vanilloid, angiotensin, and vitamin D(3) receptor sites. Drugs interfering with the nitric oxide/cGMP-cAMP pathway, Rho-kinase and COX inhibitors, as well as drugs targeting receptors and mechanisms within the CNS, are also of interest and deserving of further study for the treatment of LUTS.

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The Effect of Angiotensin Converting Enzyme Inhibition and Angiotensin II Receptor Antagonism on Obstructed Rat Bladder

Cited by 17 publications

References 28 publications

The role of angiotensin II in stress urinary incontinence: A rat model

The role of angiotensin II in stress urinary incontinence: A rat model

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

LUTS treatment: Future treatment options

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