RESUMO
INTRODUCTION AND AIM: This study evaluated the possible differences between an angiotensin converting enzyme (ACE) inhibitor and a beta-blocker concerning their potential protective role on female external genitalia in spontaneously hypertensive rats (SHR). MAIN OUTCOME MEASURES: Morphological changes in the clitoris after antihypertensive treatments. METHODS: For 6 months, SHR received no treatment; SHR + ramipril (RAM), SHR + atenolol (AT), and control Wistar Kyoto (WKY) rats received no treatment. Clitorises were processed for immunohistochemistry using anti-alpha-smooth muscle actin (alpha-SMA), anti-collagen I and III, anti-transforming growth factor beta(1) (TGFbeta(1)), and anti-endothelial nitric oxide synthase (eNOS) antibodies. RESULTS: SHR + RAM and SHR + AT presented significantly lower blood pressure in both groups vs. untreated SHR. Compared with WKY, alpha-SMA was increased in the arteries and in the cavernous spaces of the clitoris together with a marked increase in wall/lumen ratio in clitoral vessels in untreated SHR. All these alterations were diminished in SHR + AT (P < 0.01). SHR + RAM presented differences with respect to SHR + AT in the reduction of these variables. TGFbeta(1) expression in the vessel wall from the clitoris and collagen I and III deposition in the interstitium from the clitoris in untreated SHR were significantly more (P < 0.01) than in WKY. While SHR + AT showed a mild decrease in these variables, SHR + RAM presented a significant reduction (P < 0.01) in TGFbeta(1) expression interstitial fibrosis and in both types of collagens. Positive immunostaining of eNOS in the sinusoidal endothelium from the clitoris was less (P < 0.01) in untreated SHR (3.4 +/- 1.3%) and SHR + AT (5.1 +/- 1.2%) than in SHR + RAM (17.2 +/- 1.6%) and WKY (15.9 +/- 1.7%). Untreated SHR and SHR + AT presented more surrounding connective tissue at the perineurium in the clitoris (P < 0.01) than SHR + RAM. CONCLUSION: ACE inhibition provided a considerable protective role on the female external genitalia structures in SHR by a mechanism that may be, at least in part, independent of the degree of blood pressure lowering.
Assuntos
Antagonistas Adrenérgicos beta/farmacologia , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Clitóris/efeitos dos fármacos , Hipertensão/tratamento farmacológico , Antagonistas Adrenérgicos beta/administração & dosagem , Inibidores da Enzima Conversora de Angiotensina/administração & dosagem , Animais , Colágeno/metabolismo , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Feminino , Imuno-Histoquímica/métodos , Ratos , Ratos Endogâmicos WKYRESUMO
OBJECTIVE: The present study reviews the mechanism involved in the initiation and maintenance of penile erection. METHOD: The study reviews the literature on the basic concepts supporting either "magically" or scientifically the erectile mechanism. An anatomo-physiological update is also included (i.e., the main neurological, muscular, and vasculoendothelial phenomena). RESULTS: Present studies based on the vasoactive action of different drugs have increased the knowledge on the neurological, muscular, and vasculoendothelial phenomena. The cavernous muscular relaxation may start and finish due to the equilibrium between the contractile adrenergic and the relaxing non adrenergic-non cholinergic stimulus through intracellular nitric oxide synthesis. This is an essential phenomenon involved in the entry and "trapping" of blood within the sinus spaces. CONCLUSIONS: Our knowledge on the erectile mechanisms through neuromediators is increasing. The role of the endothelium in intracellular nitric oxide synthesis and its relaxing effect, will improve our understanding of both physiological and therapeutic phenomena.