Beta-Blockers in Hypertension

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Antagonism of beta-adrenergic receptors affects blood pressure through a number of mechanisms,

  • Reducing cardiac output
  • act on the juxtaglomerular complex to reduce renin secretion and thereby diminish production of circulating angiotensin II.
  • alteration of the control of the sympathetic nervous system at the level of the CNS,
  • altered baroreceptor sensitivity,
  • altered peripheral adrenergic neuron function, and
  • increased prostacyclin biosynthesis.
  1. Drugs without intrinsic sympathomimetic activity produce an initial reduction in cardiac output and a reflex-induced rise in peripheral resistance generally with no net change in arterial pressure; peripheral resistance gradually returns to pretreatment values or less.
  2. Drugs with intrinsic sympathomimetic activity produce lesser decreases in resting heart rate and cardiac output; the fall in arterial pressure correlates with a fall in vascular resistance below pretreatment levels, possibly because of stimulation of vascular b2 adrenergic receptors that mediate vasodilation.


ADVERSE EFFECTS AND PRECAUTIONS

The beta adrenergic blocking agents should be avoided in patients with

  • Asthma
  • Sinoatrial or atrioventricular (AV) nodal dysfunction, or
  • in combination with other drugs that inhibit AV conduction, such as verapamil.
  • Patients with type 1 diabetes mellitus also are better treated with other drugs (e.g., ACE inhibitors).
  • b Receptor antagonists without intrinsic sympathomimetic activity increase concentrations of triglycerides in plasma and lower those of high-density lipoprotein (HDL) cholesterol.
    b Adrenergic blocking agents with intrinsic sympathomimetic activity have little or no effect on blood lipids.
  • Sudden discontinuation of b adrenergic blockers can produce a withdrawal syndrome that is likely due to up-regulation of b receptors during blockade, causing enhanced tissue sensitivity to endogenous catecholamines; this can exacerbate the symptoms of coronary artery disease. The result, especially in active patients, can be rebound hypertension. Thus, b adrenergic blockers should be tapered over 10–14 days.
  • NSAIDs such as indomethacin can blunt the antihypertensive effect of propranolol and probably other b receptor antagonists. This effect may relate to inhibition of vascular synthesis of prostacyclin, as well as to Na+ retention.

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