see also:

• pharmacology main index
• cardiology
• beta blockers
• sympathomimetics
• benign prostatic hyperplasia (BPH)

• alpha blockers prevent the action of sympathomimetic agents such as adrenaline on the alpha adrenergic receptors

• postural hypotension and dizziness +/- reflex tachycardia
• decreased peripheral vascular resistance and lower diastolic blood pressure
• improved urine flow in those with benign prostatic hyperplasia (BPH)
• nasal stuffiness / vasodilatory rhinitis
• inability to achieve erection
• reduced libido
• retrograde ejaculation
• impaired pupil dilatation causing some blurring of vision
• decreased sweating may increase risk of heat illness in hot environments
• decreased saliva production and thus dry mouth
• fluid retention (may require a concomitant diuretic)
• impaired cardiac function and possible congestive cardiac failure in those with existing poor ejection fractions

• alfuzosin
• doxazosin
• tamsulosin
• terazosin
• see also benign prostatic hyperplasia (BPH)

• Classical alpha-1 adrenergic blocker but has alpha-2 antag. as well
  • ⇒ induces additional release of NA → tachycardia;
• Can be used in HT crisis but tachycardia may be problem in IHD;
• Uses:
  • To antagonise adrenaline-induced vasoconstriction in cases of inadvertent adrenaline use in end-artery regions;
  • As a diagnostic agent in phaeochromocytoma & as adrenolytic during Sx of this tumour;
  • Severe vasospasm in peripheral vascular disease: 10mg IM/IV 1-2/day;

• Long-acting noncomp. a-blocker,& prevents uptake of amines into neuronal & extraneuronal storage sites thus potentiating the effects of NA & adrenaline on beta-receptors;
• Also has noncompetitive blockade of histamine, 5HT & muscarinic receptors;
• Thus, decreases periph.resistance
• causes significant hypotension, nasal stuffiness, and dizziness as it blocks both a1 and a2 receptors
• Uses:
  • HT episodes in phaeochromocytoma;
  • Urinary retention due to neuropathic bladder;

• arterial, venous & pulmonary vasodilatation without signif. tachycardia;
• similar to nifedipine-type Ca antags. but has greater venous effect;
• no alpha-2 antagonism;
• does not increase intracranial pressure;
• also acts on:
  • CNS - reduces adrenergic activity;
    • ⇒ no associated sustained tachycardia;
  • CNS - serotonin agonist
    • ⇒ induces additional reduction in adrenergic activity;
    • T 1/2 = 3hrs; hepatic metabolism; plasma protein binding 80%;
• IV dose 0.5 - 2mg/kg bolus for acute elevations in BP;

• in the 1970's, became the first available selective α1-blocker for the treatment of symptomatic benign prostatic hyperplasia (BPH)
• short halflife necessitated 3 daily doses, and a high incidence of first-dose syncope resulted in poor compliance
• Decreases peripheral resistance ? due mainly to block of post-synaptic alpha receptors.
• Effect mainly at level of arterioles; The effect is more pronounced on diastolic BP;
• Unlike conventional alpha-blockers, not accompanied by reflex tachycardia!
• Rebound hypertension does not occur on abrupt withdrawal;
• May increase plasma renin in CCF;
• Beneficial in CCF (but effect may rapidly attenuate in some pts) by:
  • reducing LV filling pressure;
  • reducing cardiac impedance;
  • augments cardiac output;
• Extensively metabolised by liver & bioavailability increases 2-3x in CCF;