کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2012369 | 1067030 | 2009 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sildenafil increases the force of right atrial contractions in vitro via the NO-guanylyl cyclase pathway involving β-adrenoceptor linked mechanisms
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: Sildenafil increases the force of right atrial contractions in vitro via the NO-guanylyl cyclase pathway involving β-adrenoceptor linked mechanisms Sildenafil increases the force of right atrial contractions in vitro via the NO-guanylyl cyclase pathway involving β-adrenoceptor linked mechanisms](/preview/png/2012369.png)
چکیده انگلیسی
Sildenafil, a drug used in the treatment of erectile dysfunction, is a phosphodiesterase 5A inhibitor that increases cyclic guanosine monophosphate (cGMP) levels. In addition to its vascular actions, sildenafil is also known to alter cardiac functions. This study was undertaken to elucidate the effect of sildenafil on cardiac contractility and the underlying mechanisms. The experiments were conducted on spontaneously-beating right atria isolated from adult rats. The effect of sildenafil on the isometric contractions in vitro was examined in the absence or presence of antagonists. Sildenafil (0.001-10 μM) produced a concentration-dependent increase in the atrial force of contraction without altering the atrial rate, even up to 10 μM. A concentration as low as 0.001 μM produced a significant increase (16%) in force and the increase was about 50% at 10 μM. Pretreatment with methylene blue (a guanylyl cyclase inhibitor) or N-Ï-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor) blocked the force changes induced by sildenafil. Sildenafil-induced increase in force of contraction was also blocked by propranolol (a β-adrenoceptor antagonist) and diltiazem (an L-type Ca2+ channel antagonist). The present results demonstrate that sildenafil increases the atrial force of contraction involving cGMP-β-adrenoceptor-Ca2+ channel-dependent mechanisms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacological Reports - Volume 61, Issue 6, NovemberâDecember 2009, Pages 1146-1152
Journal: Pharmacological Reports - Volume 61, Issue 6, NovemberâDecember 2009, Pages 1146-1152
نویسندگان
Sadhana Kanoo., Shripad B. Deshpande,