Alfatam Mechanism of Action

Pharmacology: Tamsulosin hydrochloride binds selectively and competitively to postsynaptic/1-adrenoceptors, particularly to subtypes alpha1A and alpha1D. It brings about relaxation of prostatic and urethral smooth muscle.
Tamsulosin Hydrochloride 0.4 mg increases the maximum urinary flow rate. It relieves obstruction by relaxing smooth muscle in prostate and urethra. It also improves the irritative symptoms in which bladder instability plays an important role.
These effects on storage and voiding symptoms are maintained during long-term therapy.
The need for surgical treatment is significantly delayed.
α1-blockers can reduce blood pressure by lowering peripheral resistance. No reduction in blood pressure of any clinical significance was observed during studies with Tamsulosin Hydrochloride MR 0.4 mg.
Pharmacokinetics: Absorption: Tamsulosin is rapidly absorbed from the intestine and is almost completely bioavailable.
Absorption of tamsulosin is reduced by a recent meal. The patient always taking Tamsulosin Hydrochloride 0.4 mg after the same meal can promote uniformity of absorption. Tamsulosin shows linear kinetics. After a single dose of Tamsulosin Hydrochloride 0.4 mg in the fed state, plasma levels of tamsulosin peak at around 6 hours and in the steady state, which is reached by day 5 of multiple dosing, Cmax in patients is about two-thirds higher than that reached after a single dose. Although this was seen in elderly patients, the same finding would also be expected in young ones. There is a considerable inter-patient variation in plasma levels both after single and multiple dosing.
Distribution: In humans tamsulosin is about 99% bound to plasma proteins and the volume of distribution is small (about 0.2 L/kg).
Biotransformation: Tamsulosin has a low first pass effect, being metabolized slowly. Most tamsulosin is present in plasma in the form of unchanged medicine. It is metabolized in the liver. In rats, hardly any induction of microsomal liver enzymes was seen to be caused by Tamsulosin. No dose adjustment is warranted in hepatic insufficiency.
None of the metabolites are more active than tamsulosin itself.
Excretion: Tamsulosin and its metabolites are mainly excreted in the urine with about 9% of a dose being present in the form of unchanged medicine. After a single dose of Tamsulosin Hydrochloride in the fed state, and in the steady state in patients, elimination half-lives of about 10 and 13 hours respectively have been measured. The presence of renal impairment does not warrant lowering the dose.