Use of β blockers in Hypertension
Although traditionally an acceptable first-line therapy for hypertension, β-blockers (particularly atenolol, which has 72% of the clinical trial data) are not recommended by contemporary guidelines as initial therapy for patients with uncomplicated hypertension. Four possible mechanisms have been invoked for how β-blockers reduce BP:
- 1. Inhibit renin release from the juxtaglomerular apparatus of the kidney.
- 2. Diminish tonic sympathetic outflow from the central nervous system.
- 3. Reduce myocardial contractility.
- 4. Reduce cardiac output, and vasodilate (some more than others).
Some β-blockers have ancillary properties, including greater selectivity for the β1-adrenoreceptor, water solubility, intrinsic sympathomimetic activity, membrane-stabilizing activity, or other properties (e.g., α1-blocking activity, enhancement of nitric oxide bioavailability). Several β-blockers are effective second-line therapy (after ACE inhibitors) for heart failure. Adverse effects include bradycardia, fatigue, bronchoconstriction, dyspnea on exertion, and impairment of recognition of hypoglycemia in brittle diabetics. Many β-blockers decrease high-density lipoprotein cholesterol levels, raise triglycerides, and may impair glucose tolerance. They are nonetheless very useful for reducing pulse rate and BP and are often used in patients with aortic dissection, coronary disease, cardiac arrhythmias, and other selective indications.