For the treatment of symptomatic BPH and mild to moderate hypertension.
In general, &alpha;<sub>1</sub>-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. &alpha;<sub>1</sub>-Receptors are 7-transmembrane domain receptors coupled to G proteins, G<sub>q/11</sub>. Three &alpha;<sub>1</sub>-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: &alpha;<sub>1A</sub> (chromosome 8), &alpha;<sub>1B</sub> (chromosome 5), and &alpha;<sub>1D</sub> (chromosome 20). Terazosin is the first &alpha;<sub>1</sub>-receptor antagonist to demonstrate selectivity for the &alpha;<sub>1A</sub>-receptor. All three receptor subtypes appear to be involved in maintaining vascular tone. The &alpha;<sub>1A</sub>-receptor maintains basal vascular tone while the &alpha;<sub>1B</sub>-receptor mediates the vasocontrictory effects of exogenous &alpha;<sub>1</sub>-agonists. Activation of &alpha;<sub>1</sub>-receptors activates G<sub>q</sub>-proteins, which results in intracellular stimulation of phospholipases C, A<sub>2</sub>, and D. This results in mobilization of Ca<sup>2+</sup> from intracellular stores, activation of mitogen-activated kinase and PI<sub>3</sub> kinase pathways and subsequent vasoconstriction. Terozosin produces its pharmacological effects by inhibiting &alpha;<sub>1A</sub>-receptor activation. Inhibition of these receptors in the vasculature and prostate results in muscle relaxation, decreased blood pressure and improved urinary outflow in symptomatic benign prostatic hyperplasia.
LD<sub>50</sub>=259.3mg/kg (IV in mice)
Essentially completely absorbed in man (90% bioavailability).
12 hours
Approximately 10% of an orally administered dose is excreted as parent drug in the urine and approximately 20% is excreted in the feces.