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      Different Effect of Losartan and Amlodipine on Penile Structures in Male Spontaneously Hypertensive Rats

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          Background: Erectile dysfunction is highly prevalent in hypertensive patients. Since both angiotensin II receptor type-1 blockers (ARBs) and calcium antagonists are current and effective antihypertensive drugs, the aim of this study was to determine possible differences between ARBs and calcium antagonists concerning the protection of penile structures from the deleterious effects of arterial hypertension. Methods and Results: During 6 months, 3 groups of male spontaneously hypertensive rats (SHR) and 1 of Wistar-Kyoto (WKY) rats, as a control group, were studied: SHR without treatment; SHR with losartan (L) 30 mg/kg/day; SHR with amlodipine (A) 3 mg/kg/day, and WKY without treatment. Cavernous smooth muscle (CSM) and vascular smooth muscle (VSM) from cavernous arteries, cavernous tissue fibrosis and collagen type III (COL III) were evaluated. After 6 months, SHR+L and SHR+A showed a similar reduction in blood pressure compared with untreated SHR. However, only SHR+L and control WKY presented significantly lower values of: CSM (p < 0.01), VSM (p < 0.01), and COL III ( p < 0.01) when compared with either untreated SHR or SHR+A. There was also a positive correlation between left ventricular mass and proteinuria with VSM from cavernous arteries, CSM and COL III in untreated SHR and SHR+A. These relations were not present in SHR+L and WKY. Conclusion: Although losartan and amlodipine achieved similar blood pressure control, losartan but not amlodipine showed a significant protective role against structural changes in the vessels and cavernous spaces of the erectile tissue caused by arterial hypertension.

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          Hypertension is associated with severe erectile dysfunction.

          The prevalence and severity of erectile dysfunction in patients with hypertension need to be further evaluated. We evaluate medical and hypertension status, and erectile function in patients with hypertension. The International Index of Erectile Function, which is a detailed questionnaire, including well established components to evaluate patient medical history, hypertension status and erectile dysfunction, was mailed to 476 male patients of the outpatient Hypertension Center of Columbia Presbyterian Medical Center. The questionnaire was completed by 104 (22.3%) patients, and mean age was 62.2 years (range 34 to 75). Of the patients 84.8% were sexually active and 68. 3% had various degrees of erectile dysfunction, which was mild in 7. 7%, moderate in 15.4% and severe in 45.2%. Compared to the general population of erectile dysfunction cases in the literature our study population with hypertension had a higher incidence of severe erectile dysfunction. Although correlations of antihypertensive medications with incidence of erectile dysfunction did not reach statistical significance, there was a clear trend with patients treated with diuretics and beta-blockers having the highest incidence and those treated with alpha-blockers having the lowest incidence of erectile dysfunction. In addition to the observation that erectile dysfunction is more prevalent in patients with hypertension than in an age matched general population, our study shows that it is more severe in those with hypertension than in the general population.
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            Ca2+ channel blockers modulate metabolism of collagens within the extracellular matrix.

            The extracellular matrix (ECM) is an intricate network composed of an array of macromolecules capable of regulating the functional responsiveness of cells. Its composition greatly varies among different types of tissue, and dysregulation of its metabolism may contribute to vascular remodeling during the pathogenesis of various diseases, including atherosclerosis. In view of their antiatherosclerotic effects, the role of Ca2+ channel blockers in the metabolism of ECM was examined. Nanomolar concentrations of the five Ca2+ channel blockers amlodipine, felodipine, manidipine, verapamil, or diltiazem significantly decreased both the constitutive and platelet-derived growth factor BB-dependent collagen deposition in the ECM formed by human vascular smooth muscle cells and fibroblasts. The drugs inhibited the expression of fibrillar collagens type I and III and of basement membrane type IV collagen. Furthermore, Ca2+ channel blockers specifically increased the proteolytic activity of the 72-kDa type IV collagenase as shown by gelatin zymography and inhibited the transcription of tissue inhibitor of metalloproteinases-2.
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              Effects of enalapril and amlodipine on small-artery structure and composition, and on endothelial dysfunction in spontaneously hypertensive rats.

              To determine whether an angiotensin converting enzyme inhibitor, enalapril, and a dihydropyridine calcium channel antagonist, amlodipine, regress the altered structure, media composition, and vascular relaxation of small arteries of spontaneously hypertensive rats. Spontaneously hypertensive rats aged 10 weeks were treated for 12 weeks with 10 mg/kg per day enalapril or 10-20 mg/kg per day amlodipine and compared with age-matched untreated spontaneously hypertensive rats. Small coronary, renal, mesenteric, and femoral arteries (lumen diameter 200-250 microm) were studied isometrically on a wire myograph, and mesenteric arteries isobarically as pressurized vessels. The composition of the vascular media of the latter was studied by electron microscopy. Blood pressure, and cardiac and aortic hypertrophy were reduced in treated spontaneously hypertensive rats. Treatment significantly decreased media thickness and media: lumen ratio of coronary, renal, mesenteric, and femoral small arteries studied isometrically and of pressurized mesenteric small arteries. Media cross-sectional area was smaller for coronary arteries studied isometrically and mesenteric arteries studied isobarically. Electron microscopic analysis revealed an increase in collagen: elastin ratio in the media of spontaneously hypertensive rat vessels, and a decrease under treatment to levels found in Wistar-Kyoto rats, with no significant changes detected in smooth muscle cells. The amplitude of contractions induced by acetylcholine on wire-myograph-mounted mesenteric arteries from spontaneously hypertensive rats were decreased by treatment, and relaxation of pressurized arteries induced by acetylcholine was normalized. Treatment of spontaneously hypertensive rats with enalapril or with amlodipine resulted in regression of cardiovascular hypertrophy and amelioration of endothelial dysfunction. Morphometric results obtained using an isometric myograph and a pressurized preparation to study rat small arteries were closely correlated. Regression of structural remodeling in small arteries was outward hypotrophic, with a reduction in the collagen: elastin ratio, and without net change in the absolute and relative volumes of smooth muscle and number of smooth muscle layers.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                December 2004
                28 February 2005
                : 24
                : 6
                : 614-623
                aLaboratory of Experimental Medicine, Hospital Alemán, and bInstituto de Investigaciones Cardiológicas, Buenos Aires, Argentina
                82598 Am J Nephrol 2004;24:614–623
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 8, Tables: 1, References: 29, Pages: 10
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                Original Report: Laboratory Investigation


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