Doxazosin mesylate is a quinazoline compound sold by Pfizer under the brand name CARDURA. CARDURA is indicated for the treatment of both the urinary outflow obstruction and obstructive and irritative symptoms associated with BPH: obstructive symptoms (hesitation, intermittency, dribbling, weak urinary stream, incomplete emptying of the bladder) and irritative symptoms (nocturia, daytime frequency, urgency, burning). CARDURA may be used in all BPH patients whether hypertensive or normotensive. In patients with hypertension and BPH, both conditions were effectively treated with CARDURA monotherapy. CARDURA provides rapid improvement in symptoms and urinary flow rate in 66–71% of patients. CARDURA is also indicated for the treatment of hypertension. CARDURA may be used alone or in combination with diuretics, beta-adrenergic blocking agents, calcium channel blockers, or angiotensin-converting enzyme inhibitors. Doxazosin acts by inhibiting the postsynaptic alpha(1)-adrenoceptors on vascular smooth muscle. This inhibits the vasoconstrictor effect of circulating and locally released catecholamines (epinephrine and norepinephrine), resulting in peripheral vasodilation.

Prazosin (trade names Minipress, Vasoflex, Lentopres, and Hypovase) is a selective α-1-adrenergic receptor antagonist used to treat hypertension. Prazosin acts by inhibiting the postsynaptic alpha-1-adrenoceptors on vascular smooth muscle. This inhibits the vasoconstrictor effect of circulating and locally released catecholamines (epinephrine and norepinephrine), resulting in peripheral vasodilation. Prazosin is orally active and has a minimal effect on cardiac function due to its alpha-1 receptor selectivity. However, when prazosin is started, heart rate and contractility go up in order to maintain the pre-treatment blood pressures because the body has reached homeostasis at its abnormally high blood pressure. The blood pressure lowering effect becomes apparent when prazosin is taken for longer periods of time. The heart rate and contractility go back down over time and blood pressure decreases. The antihypertensive characteristics of prazosin make it a second-line choice for the treatment of high blood pressure. Prazosin is also useful in treating urinary hesitancy associated with prostatic hyperplasia, blocking alpha-1 receptors, which control constriction of both the prostate and urethra. Although not a first line choice for either hypertension or prostatic hyperplasia, it is a choice for patients who present with both problems concomitantly. Common (4–10% frequency) side effects of prazosin include dizziness, headache, drowsiness, lack of energy, weakness, palpitations, and nausea. Less frequent (1–4%) side effects include vomiting, diarrhea, constipation, edema, orthostatic hypotension, dyspnea, syncope, vertigo, depression, nervousness, and rash.

Bethanidine is a post-ganglionic adrenergic neurone-blocking agent which exerts a marked postural hypotensive effect. The precise mechanism whereby bethanidine causes blockade of adrenergic neurones is unknown. An initial sympathomimetic effect has been demonstrated in man and animals, possibly due to release of catecholamines.

Debrisoquin is an antihypertensive drug having guanethidine-like properties, which inhibits monoamine oxidase (MAO) and does not enter the brain. Debrisoquine was used for the treatment of hypertension. Debrisoquine hydroxylation phenotype has been the most used test in humans to evaluate CYP2D6 activity. Two debrisoquine hydroxylation phenotypes have been described: poor and extensive metabolizers. A group with a very low debrisoquine metabolic ratio within the extensive metabolizers, named ultrarapid metabolizers, has also been distinguished. This CYP2D6 variability can be for a large part alternatively determined by genotyping, which appears to be of clinical importance given CYP2D6 involvement in the metabolism of a large number of commonly prescribed drugs.

Trimazosin was originated by Pfizer and was licensed to Bristol-Myers Squibb worldwide except for Canada, Mexico and the USA. Trimazosin is a quinazoline antihypertensive agent structurally related to the selective alpha 1-adrenoceptor blocker prazosin. Trimazosin is an alpha adrenergic receptor antagonist. Compared with prazosin, trimazosin was a less potent but more efficacious hypotensive agent. At doses which caused equal or even greater hypotensive effects than those caused by prazosin, trimazosin caused less inhibition of pressor responses to phenylephrine. When administered during a maximum hypotensive response to prazosin, trimazosin caused an additional fall in pressure. Trimazosin is an effective antihypertensive when given by itself or in combination with a diuretic. Its ability to induce vasodilation without concomitant sodium retention or stimulation of the renin axis may be an important factor in its effectiveness. Trimazosin has the potential to cause sustained improvement in left ventricular function, both at rest and during exercise, in patients with chronic congestive heart failure (CHF).

Urapidil is an anti-hypertensive agent approved in Europe for the treatment of the corresponding disease. The drug acts by activating 5HT1a receptor and inhibiting alpha1-adrenergic receptors.

Guanoxan is 2-guanidinomethylbenzo-1,4-dioxan. It acts as a blocker of alpha-2 adrenoceptors. The clinical use of this drug has been in the treatment of hypertension. Both systolic and diastolic pressures are lowered in the lying and standing positions.

Guanazodine is a new antihypertensive drug. Guanazodine caused a sustained decrease in the systemic blood pressure of spontaneously hypertensive rats, renal hypertensive dogs and normal cats. No tachyphylaxis developed when the drug was administered orally. The heart rate decreased. Guanazodine relaxed the cat nictitating membrane, attenuated the positive chronotropic response to sympathetic nerve stimulation in anesthetized dogs and in isolated rabbit aorta to transmural electrical stimulation. Guanazodine potentiated the pressor response to noradrenaline but attenuated the response to tyramine in anesthetized cats. It may be concluded that the hypotensive effect of guanazodine is related to adrenergic neuron blocking action, the noradrenaline-depleting action in peripheral tissues is similar to the effect of guanethidine and bethanidine. However, this drug is less potent than guanethidine. Toxicity and side effects appear to be less with guanazodine than with guanethidine and bethanidine.

Guanoclor is an anti-hypertensive agent developed by Pfizer Ltd. (U.K.). It seems to be effective in various types of hypertension (unknown aetiology, renal, and malignant). It affects both systolic blood-pressure and diastolic blood-pressure. It is an adrenergic neurone-blocking agent, which also interferes with noradrenaline synthesis by inhibition of the enzyme dopamine beta-hydroxylase. Clinical use of the compound was first reported by Lawrie et al. (1964), who achieved satisfactory blood-pressure control in 60% of their cases with guanoclor alone, and in a further 18% with the addition of a thiazide diuretic. They also noted a significant reduction in urinary noradrenaline levels during guanoclor administration. Guanochlor has an affinity for the Na+/H+ exchanger ranging between 0.5 uM and 6 uM in different systems and is more potent than amiloride in all systems studied. It is suggested that guanochlor recognizes a binding site on the Na+/H+ exchanger that is distinct from the amiloride binding site.

Guanoxabenz is an antihypertensive drug that was in clinical use in the 1980s. It acts as a selective agonist of alpha2A1 and alpha2B1 adrenergic receptors. Guanoxabenz is the main metabolite of the FDA-approved drug guanabenz.