Milironin has following except:
a- +ve inotropic
b- vasodilator
c- increase ca intercellular***
d- phosphodiasterase inhibitor
e- potantiate the effect of CAMP
-----------------------------------
In clinical and experimental cardiology, phosphodiesterase-5 (PDE-5) inhibitors have attracted scientific interest in recent years as a therapeutic tool for the treatment of PAH. Phosphodiesterases are a superfamily of enzymes that inactivate cyclic adenosine monophosphate and cyclic guanosine monophosphate, the second messengers of prostacyclin and nitric oxide. The reasoning for using PDE-5 inhibitors in PAH is based on their relative selectivity for pulmonary circulation and their ability to overexpress the nitric oxide pathway by inhibiting hydrolysis of cyclic guanosine monophosphate and increasing its concentrations, which produces vasodilator, antiproliferative and proapoptotic effects that can reverse pulmonary vascular remodeling. In addition, they can increase right ventricular inotropism by increasing cyclic adenosine monophosphate mediated by the inhibition of cyclic guanosine monophosphate sensitive type 3 phosphodiesterase.
Sildenafil, tadalafil and vardenafil are 3 PDE-5 inhibitors currently in clinical use that share a similar mechanism of action although they show some significant differences in potency, selectivity for PDE-5 and pharmacokinetic properties.
For the treatment of PAH in patients in functional class II and III (NYHA / WHO), sildenafil was approved by the Food and Drug Administration and the European Medicines Agency in 2005; and tadalafil by the Food and Drug Administration and the European Medicines Agency in 2009. In Mexico, sildenafil and tadalafil were approved by the Federal Commission for Protection against Health Risks for the same indication in 2010 and 2011 respectively.
a- +ve inotropic
b- vasodilator
c- increase ca intercellular***
d- phosphodiasterase inhibitor
e- potantiate the effect of CAMP
-----------------------------------
In clinical and experimental cardiology, phosphodiesterase-5 (PDE-5) inhibitors have attracted scientific interest in recent years as a therapeutic tool for the treatment of PAH. Phosphodiesterases are a superfamily of enzymes that inactivate cyclic adenosine monophosphate and cyclic guanosine monophosphate, the second messengers of prostacyclin and nitric oxide. The reasoning for using PDE-5 inhibitors in PAH is based on their relative selectivity for pulmonary circulation and their ability to overexpress the nitric oxide pathway by inhibiting hydrolysis of cyclic guanosine monophosphate and increasing its concentrations, which produces vasodilator, antiproliferative and proapoptotic effects that can reverse pulmonary vascular remodeling. In addition, they can increase right ventricular inotropism by increasing cyclic adenosine monophosphate mediated by the inhibition of cyclic guanosine monophosphate sensitive type 3 phosphodiesterase.
Sildenafil, tadalafil and vardenafil are 3 PDE-5 inhibitors currently in clinical use that share a similar mechanism of action although they show some significant differences in potency, selectivity for PDE-5 and pharmacokinetic properties.
For the treatment of PAH in patients in functional class II and III (NYHA / WHO), sildenafil was approved by the Food and Drug Administration and the European Medicines Agency in 2005; and tadalafil by the Food and Drug Administration and the European Medicines Agency in 2009. In Mexico, sildenafil and tadalafil were approved by the Federal Commission for Protection against Health Risks for the same indication in 2010 and 2011 respectively.
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pharmac