Drugs NOT used in pulmonary hypertension

Drug NOT used in pulmonary hypertension

a) Calcium channel blocker
b) Endothelin receptor antagonist
c) Alpha blocker
d) Prostacyclin
Correct Answer - C
alpha blockers [Ref- Harrison 17th/e p 1577, 1578] Pulmonary
hypertension
General management
Diuretic therapy may be useful as it relieves pulmonary edema.
Anticoagulant therapy is advocated for all patients.
Specific management
Calcium channel blockers
Patients who have substantial reductions in pulmonary arterial
pressure in response to short acting vasodilators at the time of
cardiac catheterization should he initially treated with calcium
channel blockers.
Endothelin receptor antagonist
Bostenan is a non-selective endothelium receptor antagonist, is an
approved t/t ,for patients who are NYHA .functional classes III and
IV.
Phosphodiesterase-5 inhibitors
Slidenafil is used for patients who are NYHA functional classes II
and
Prostacyclins
Iloprost is a prostacyclin analogue used in PAH patients who are
NYHA functional classes III and IV.
Pulmonary circulation is unique in that it accommodates a blood flow
that is almost equal to that of all the other organs of body but still
maintains low pressure.
The factors responsible for low pressure in pulmonary circulation
(even with large volume of blood) are:- - Larger diameter of
pulmonary vessels due to thin wall of pulmonary artery and
arterioles.

  • Greater compliance (distensibility) of pulmonary vessels.
    numoral factors responsible for maintaining pulmonary circulation:?
    Normally
    NO causes vosodilation and proliferation of smooth muscles by r in
    the conc. of cGMP —) this increases the diameter of pulmonary
    vessels.
    causes vosodilation and decreased proliferation of smooth muscles
    by increasing the conc. of cAMPincrease in the diameter of
    pulmonary vessels. Prostaglandin also decreases coagulation.
    Endothelin causes vasoconstriction and increase smooth muscle
    proliferation si lumen of pulmonary vessels. - Normally the
    vasodilators and antiprolifeave effects of NO and PGI7 dominate
    In Pulmonary hypertension
    There is l production of NO (and cGMP) and PGI2 (and cAMP), t
    vasoconstriction and proliferation of smooth
    muscles, st lumen of pulmonary vessel. Decreased production of
    PGI2 also causes increased coagulation.
    There is T production of endothelin, /vasoconstriction and smooth
    muscle proliferation, .1 lumen.
    Drug therapy in puhnonan, hypertension is targetted at these growth
    factor pathways which are involved in the pathogenesis of
    pulmonary hypertension:
    Endothelium receptor antagonist
    Bostenan is an endothelin receptor antagonist. It prevents
    endothelin mediated contraction of vessels. Phosphodiesterase-5

inhibitors
Nitric oxide mediates its action through increasing cGMP
concentration. Increased cGMP relaxes the vessels. cGMP is
degraded by an enzyme phosphodiesterase-5 (PDE-5).

  • Slidenafanil is a phosphodiesterase 5 inhibitor. It reduces the
    degradation of cGMP, thus causing vascular relaxation and reducing
    pulmonary hypertension.
    Prostacyclins
    In pulmonary hypertension, the level of prostacycline is reduced.
    This causes pulmonary constriction as prostacyclin causes dilatation
    of pulmonary vessels.