2005
DOI: 10.1016/j.eururo.2005.06.017
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Activity of Angiotensin Peptides in Clitoral Cavernosum of Alloxan Induced Diabetic Rabbit

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Cited by 7 publications
(5 citation statements)
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“…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: 66%
See 1 more Smart Citation
“…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: 66%
“…In addition, Ang I may be acted upon by chymase (a chymotrypsin-like serine protease released from mast cells) in an alternative catalysis pathway, producing Ang II. plasminogen activator can also catalyze the conversion of Ang I to Ang II (Park et al 2005a;Toblli et al 2007). Ang II is converted to angiotensin III via aminopepsidase A and is then further metabolized to angiotensin IV by aminopepsidase N, and ultimately to the inactive angiotensin 1-7 (Tipnis et al 2000).…”
Section: Synthesis Of Angiotensin IImentioning
confidence: 97%
“…Interestingly, erectile tissue from the Zucker obese rat exhibited also changes in the activities of Protein kinase C (PKC) and Rho‐kinase, enhanced vasoconstrictive responses and reduced relaxations to NO donor, whereas no changes in NOS activities were observed [218]. Histological and functional studies of isolated vaginal and clitoral tissues in diabetic mice, rats, and rabbits have reported reduced epithelial thickness and atrophy of the muscularis layer, fibrosis and increased amounts of TGF‐β1, reduced vaginal levels of Endothelilal Nitric Oxide Synthase (eNOS) and arginase, reduced neuronal NOS activity, elevated levels of cGMP‐dependent protein kinase (PKG), signs of oxidative stress, reduction in estrogen receptor activities and altered sensitivities to activation of angiotensin receptors [219–221]. In vivo, the vaginal blood flow response to pelvic nerve stimulation was significantly reduced in diabetic rats and mean baseline flaccid and peak clitoral cavernous blood flows were significantly decreased in the diabetic rabbits compared with the control groups [222,223].…”
Section: Experimental Models Of Pathophysiological Statesmentioning
confidence: 99%
“…For example, clitoral blood flow and clitoral cavernosal smooth muscle content is reduced in diabetic rabbits [76]. Furthermore, clitoral corpus cavernosum tissue from diabetic rabbits exhibits increased contraction to angiotensin peptides [77]. In a small clinical study, diabetic women (N = 30) experienced decreased sensation in the clitoris, labia, and vagina, as well as at extragenital sites, compared with non‐diabetic women (N = 20) [9].…”
Section: Diabetes Female Sexual Dysfunction and Estrogenmentioning
confidence: 99%