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Alpha 1 blockers cause vasodilation by relaxing smooth muscles that control blood vessel diameter, leading to lower blood pressure. [1] FDA-approved uses of these drugs include treating conditions like benign prostatic hyperplasia, hypertension, pheochromocytoma, extravasation management, and reversal of local anesthesia.
Norepinephrine Epinephrine. A norepinephrine reuptake inhibitor (NRI, NERI) or noradrenaline reuptake inhibitor or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a reuptake inhibitor for the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline) by blocking the action of the norepinephrine transporter (NET).
These drugs inhibit the uptake of the neurotransmitter 5-HT by blocking the SERT, thus increasing its synaptic concentration, and have shown to be efficacious in the treatment of depression, however sexual dysfunction and weight gain are two very common side-effects that result in discontinuation of treatment.
The combination of beta blockers and antihypertensive drugs will work on different mechanism to lower blood pressure. [17] For example, the co-administration of beta-1 blocker atenolol and ACE inhibitor lisinopril could produce a 50% larger reduction in blood pressure than using either drug alone.
This property of SNRIs might be used to reduce doses of other pain relieving medication and lower the frequency of safety, limited efficacy and tolerability issues. [45] Clinical research data have shown in patients with GAD that the SNRI duloxetine is significantly more effective than placebo in reducing pain-related symptoms of GAD, after ...
This is a list of adrenergic drugs. These are pharmaceutical drugs , naturally occurring compounds and other chemicals that influence the function of the neurotransmitter epinephrine (adrenaline). Receptor ligands
Guanethidine, an adrenergic release inhibitor.. Adrenergic release inhibitors are a class of drugs which inhibit the release of epinephrine (adrenaline) and/or norepinephrine (noradrenaline) from adrenergic nerve terminals and are used as antihypertensives.
The main metabolite formed is 4-hydroxyatomoxetine, which glucuronate rapidly. 4-hydroxyatomoxetine is equivalent to atomoxetine but is much lower in plasma. [8] The mean elimination half-life of atomoxetine after oral administration is 3.6 hours in individuals in extensive metabolism and 21 hours in those with a slow metabolism.