Captopril reduces deposition of collagen in lamina propria and muscular layers of the bladder and ureter in neonatal dogs with partial urethral obstruction

Shirazi, Mehdi; Noorafshan, Ali; Bahri, Mohammad Arabzadeh; Hassanpoor, Abbas

doi:10.1080/00365590801905984

Cited by 6 publications

(12 citation statements)

References 22 publications

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“…Angiotensin II has been linked to a functional role in bladder contraction and smooth muscle tone in multiple species [4–6]. The present results show that AT‐1 receptor antagonism indeed inhibits the increase in NVCs that normally occurs after BOO in the mouse model – analogous to detrusor overactivity in men with BPE.…”

Section: Discussionsupporting

confidence: 54%

“…Shirazi et al. [6] showed that ang II inhibition prevented collagen deposition but did not significantly affect detrusor muscular content in a canine model of BOO. It appears that the functional role of ang II as a mediator of detrusor smooth muscle hypertrophy and fibrosis may vary by species and by specific pharmacological agent and dosage.…”

Section: Discussionmentioning

confidence: 99%

“…Local renin angiotensin systems (RASs) are common, if not ubiquitous, throughout the human body [3], and have been identified in the genitourinary tract, specifically within the bladder [4]. Investigations of human, canine and rabbit bladder muscle strips have confirmed that angiotensin II (ang II) is indeed involved in bladder contraction and smooth muscle tone [5–7]. This contractile affect of ang II appears to be mediated by the ang II type I receptor (AT‐1) [7].…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II type 1 (AT‐1) receptor inhibition partially prevents the urodynamic and detrusor changes associated with bladder outlet obstruction: a mouse model

Comiter

Phull

2011

BJU International

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8 4 1What ' s known on the subject? and What does the study add? Angiotensin II is the main effector peptide in the bladder local renin-angiotensin system. This experiment demonstrates the role of this local renin-angiotensin system with respect to bladder outlet obstruction. OBJECTIVE• To determine if treatment with an angiotensin II type 1 (AT-1) receptor antagonist, losartan, can prevent the structural and functional changes that occur in a mouse model of bladder outlet obstruction (BOO). MATERIALS AND METHODS• Twenty-four Balb/CAN mice underwent partial urethral obstruction for 6 weeks.• Twelve mice were given oral losartan (10 mg/kg/day), and 12 were not. Six mice served as unobstructed controls, and six unobstructed mice were given oral losartan (10 mg/kg/day) to determine the effect of angiotensin II inhibition on the normal bladder.• Bladder capacity (C), detrusor pressure during voiding (Pdet) and volume at fi rst non-voiding contraction (NVC1) as a percentage of C were recorded after 6 weeks.• Bladders were stained with haematoxylin and eosin for measurement of detrusor muscular thickness, and graded as 1 = atrophy ( < 100 μ m thick), 2 = normal (100 -200 μ m thick), 3 = hypertrophy ( > 200 μ m thick) compared with controls. RESULTS• Compared with controls, BOO mice had greater C (153.5 ± 20.9 vs 57.5 ± 7.4 μ l, P < 0.01), higher Pdet (28.8 ± 2.1 vs 12.1 ± 2.1 mm Hg), lower NVC1 (median = 24% vs 54% P = 0.03). BOO mice manifested greater bladder weight (93.2 ± 11.7 mg vs 26.8 ± 2.40 mg, P < 0.01) and greater detrusor muscle thickness (median 3 vs 2, P = 0.02).• Compared with untreated BOO mice, mice treated with losartan had greater mean C (248.8 ± 28.6 vs 153.5 ± 20.9 μ L, P = 0.01), no signifi cant change in mean Pdet (24.7 ± 1.6 vs 28.8 ± 2.1 mm Hg, P = 0.2) and a higher mean NVC1 (47% vs 24%, P = 0.02).• Treatment with losartan mediated an insignifi cant reduction in mean bladder weight (68.1 ± 9.1 mg vs 93.2 ± 11.7 mg, P = 0.10), but a signifi cant reduction in detrusor muscle thickness (median 2 vs 3, P = 0.02). Losartan did not mediate any signifi cant structural or functional changes in the unobstructed mouse bladder. CONCLUSION• In a mouse model of BOO, treatment with an AT-1 antagonist partially prevented the urodynamic and structural changes that otherwise occur with BOO. KEYWORDSangiotensin II , bladder outlet obstruction , benign prostatic enlargement , detrusor overactivity , detrusor hypertrophy Study Type -Therapy (case control) Level of Evidence 3b

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Angiotensin II type 1 (AT‐1) receptor inhibition partially prevents the urodynamic and detrusor changes associated with bladder outlet obstruction: a mouse model

Comiter

Phull

2011

BJU International

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“…In contrast, telmisartan, which has a longer plasma half-life and slower receptor dissociation, was indeed able to attenuate bladder muscle hypertrophy (Yamada et al 2009). In a canine model, Shirazi et al (2008) showed that Ang II inhibition did, in fact, prevent collagen deposition in the bladder, but did not significantly affect detrusor muscular content in the setting of BOO. Most recently, Comiter and Phull (2011) demonstrated that chronic AT1 receptor antagonism with losartan, at the time of BOO, did in fact partly prevent the hypertrophic changes that otherwise occurred in a rat model of urethral obstruction.…”

Section: Local Renin-angiotensin Systemsmentioning

confidence: 97%

Local renin–angiotensin systems in the genitourinary tract

Comiter¹

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Local renin-angiotensin systems are common throughout the human body. Recent evidence supports the existence of such local renin-angiotensin systems in the penis, clitoris, bladder, ureter, internal anal sphincter, and urethral sphincter. Beyond its role in regulating blood pressure through its effects on vascular tone, sodium balance, and fluid homeostasis, angiotensin II serves a key role in affecting physiologic and pathophysiologic activities of the genitourinary tract. Just as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are used for the treatment and prevention of heart disease and vascular disease, inhibition of excessive angiotensin II activity may be potentially useful for the treatment of urologic disorders.

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“…In neonatal dogs with urethral obstruction, the use of angiotensin converting enzyme inhibitor captopril decreased the collagen content of the lamina propria and muscular layer in the ureter. [13]…”

Section: Effect Of Posterior Urethral Valves On Bladder Developmentmentioning

confidence: 99%

Etiopathogenesis and management of bladder dysfunction in patients with posterior urethral valves

Thomas

2010

Indian J Urol

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Posterior urethral valves are the commonest cause of urethral obstruction in a male child. It has significant effects on the development of upper urinary tracts and in the evolution of urinary bladder function. The effect on the kidneys and the urinary bladder persists even after the successful management of the obstructing valves. A detailed evaluation of the associated bladder dysfunction will help in planning management protocols that will improve the long-term outcome of these patients.

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Captopril reduces deposition of collagen in lamina propria and muscular layers of the bladder and ureter in neonatal dogs with partial urethral obstruction

Abstract: Administration of captopril decreases the collagen content of the lamina propria and muscular layer in the ureter and bladder of neonatal dogs with PUO.

Cited by 6 publications

References 22 publications

Angiotensin II type 1 (AT‐1) receptor inhibition partially prevents the urodynamic and detrusor changes associated with bladder outlet obstruction: a mouse model

Angiotensin II type 1 (AT‐1) receptor inhibition partially prevents the urodynamic and detrusor changes associated with bladder outlet obstruction: a mouse model

Local renin–angiotensin systems in the genitourinary tract

Etiopathogenesis and management of bladder dysfunction in patients with posterior urethral valves

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