Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Toblli, Jorge Eduardo; Stella, Inés; Mazza, Osvaldo; Ferder, León; Inserra, Felipe

doi:10.1038/sj.ijir.3901146

Cited by 12 publications

(7 citation statements)

References 45 publications

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“…Moreover, AT1 activation mediates an increase in RhoA/ Rho-kinase activity and a decrease in eNOS protein expression, which can be readily reversed by the AT1 antagonist losartan (Jin 2009). This effect is specifically related to Ang II, which is supported by the finding that other antihypertensive agents did not improve erectile function (Toblli et al 2004a;Mazza et al 2006). Similar findings have been demonstrated in rat models of agerelated ED (in normotensive animals), with losartan improving eNOS protein expression and erectile function (Park et al 2005a), and in diabetic ED-with improvement following valsartan administration.…”

Section: Local Renin-angiotensin Systemssupporting

confidence: 76%

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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Section: Local Renin-angiotensin Systemssupporting

confidence: 76%

Local renin–angiotensin systems in the genitourinary tract

Comiter¹

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Angiotensin II and angiotensin I (precursor of angiotensin II) cause contraction of the corpus cavernosum smooth muscle of rabbit in a dosedependent manner and the effect of angiotensin I is attenuated by captopril, an ACEi [59]. In rats, candesartan cilexetil, an angiotensin II receptor blocker has been shown to have a significant protective role against high blood pressure-related morphologic changes in vessels and cavernous spaces of the erectile tissue [60]. Becker et al [61] observed that angiotensin II plasma levels are generally elevated in the systemic and cavernous blood of patients with an organogenic etiology of ED.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Sexual Function in Hypertensive Men Receiving Treatment: A Review of Current Guidelines Recommendation

Karavitakis

Komninos

Theodorakis

et al. 2011

The Journal of Sexual Medicine

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Introduction It has been suggested that some classes of antihypertensive drugs may induce or exacerbate sexual and/or erectile dysfunction (ED) more than others. Sexually related side effects of antihypertensive treatment may compromise patient's and partner's quality of life. Often, these side effects can lead to withdrawal or poor compliance with therapy resulting in abnormal blood pressure and associated morbidity. Aim The aim of this study was to evaluate whether hypertension clinical practice guidelines (CPGs) address ED and/or other sexual issues as either an adverse outcome of chosen therapy or as a factor to consider in treatment decision. Methods Hypertension CPGs were identified by searching PubMed (from 2000 to current), the World Wide Web, bibliographies of retrieved guidelines, and official home pages of major medical societies. Main Outcome Measures The main outcome measures used for this study were guidelines assessment using a set of author-determined survey questions. Results Twelve CPGs were identified and analyzed. From these 12, only three emphasized the importance of assessing sexual function prior to initiation and/or follow-up of antihypertensive therapy; only five described potential sexual side effects associated with some drugs; only two provided specific management recommendations on commencing antihypertensive therapy in sexually active men or those with preexisting ED and address the timeline of the potential drug-induced impairment of sexual function. Conclusions Only a minority of CPGs for the treatment of hypertension consider ED or other sexual issues as either an adverse outcome or as a factor to consider in treatment. Sexual function is an important aspect of quality of life for both the individual and his partner. It is therefore imperative to select therapy with the least possible potential for causing sexual sequelae and enable the best achievable balance between therapeutic efficacy, quality of life, and therapeutic compliance. Based on these results, our proposed algorithm attempts to effectively apply available evidence to clinical practice.

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“…Additionally, angiotensin II (Ang II) receptor subtype AT1 seems to be important in the regulation of penile erection [11]. Recently, it has been reported that an interaction against RAS can control the remodeling process in the erectile tissue in animals with arterial hypertension [12–14].…”

Section: Introductionmentioning

confidence: 99%

Differences Between Candesartan and Hydralazine in the Protection of Penile Structures in Spontaneously Hypertensive Rats

Mazza

Angerosa

Becher

et al. 2006

The Journal of Sexual Medicine

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Introduction Previous studies indicate that angiotensin type I receptor antagonists present a beneficial effect on penile structures in hypertensive rats. However, at present there is no substantial information concerning the functional aspect of this class of antihypertensive drugs. Aim To determine, by in vitro studies, functional effects of Candesartan in comparison with a traditional vasodilating agent, Hydralazine, on penile structures in a rat model of arterial hypertension. Methods During 4 months, three groups of male spontaneously hypertensive rats (SHR) and one of Wistar–Kyoto (WKY) rats, as control group, were studied: SHR without treatment; SHR with Candesartan cilexetil 7.5 mg/kg/day; SHR with Hydralazine 50 mg/kg/day; and WKY rats without treatment. Cavernous smooth muscle strips were mounted in an organ bath system for in vitro studies. In addition, cavernous smooth muscle and vascular smooth muscle from cavernous arteries, cavernous tissue fibrosis, and collagen type III were also evaluated by immunohistochemistry. Results After 4 months, SHR with Candesartan and Hydralazine showed similar reduction in blood pressure compared with untreated SHR. However, in vitro studies revealed that SHR with Candesartan displayed a better relaxation response to acetylcholine than SHR and SHR with Hydralazine (P < 0.01). Immunostaining indicates that only SHR with Candesartan and control WKY rats showed significantly lower values of: (i) cavernous smooth muscle (P < 0.01); (ii) vascular smooth muscle (P < 0.01); and (iii) collagen type III (P < 0.01) when compared with untreated SHR or SHR with Hydralazine. Additionally, SHR with Candesartan presented a higher endothelial nitric oxide synthase expression in sinusoidal endothelium in comparison with SHR, and SHR with Hydralazine (P < 0.01). Conclusion Candesartan presented equivalent blood pressure control compared with Hydralazine. However, only Candesartan showed a significant better response to acetylcholine, in in vitro studies, with a protective role against structural changes in vessels as well as in cavernous spaces of the erectile tissue.

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Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

Cited by 12 publications

References 45 publications

Local renin–angiotensin systems in the genitourinary tract

Local renin–angiotensin systems in the genitourinary tract

Evaluation of Sexual Function in Hypertensive Men Receiving Treatment: A Review of Current Guidelines Recommendation

Differences Between Candesartan and Hydralazine in the Protection of Penile Structures in Spontaneously Hypertensive Rats

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