|Systematic (IUPAC) name|
|Biological half-life||14-24 hours|
|Excretion||Renal and fecal (unchanged)|
|ATC code||C07AA12 (WHO)|
|Molar mass||309.401 g/mol[[Script error: No such module "String".]]|
|Script error: No such module "collapsible list".|
Nadolol is polar and hydrophilic, with low lipid solubility.
Nadolol is a non-selective beta blocker; that is, it non-selectively blocks both beta-1 and beta-2 receptors. It has a preference for beta-1 receptors, which are predominantly located in the heart, thereby inhibiting the effects of catecholamines and causing a decrease in heart rate and blood pressure. Its inhibition of beta-2 receptors, which are mainly located in the bronchial smooth muscle of the airways, leads to airway constriction similar to that seen in asthma. Inhibition of beta-1 receptors in the juxtaglomerular apparatus of the kidney inhibits the renin-angiotensin system, causing a decrease in vasoconstriction and a decrease in water retention. Nadolol's inhibition of beta-1 receptors in the heart and kidney lead to its effects on lowering blood pressure.
Nadolol is indicated for treatment of moderate hypertension and chest pain and supraventricular tachycardia. In patients with severe hypertension, nadolol can also treat reflex tachycardia due to treatment with vasodilators. Nadolol and other non-selective beta-blockers are used in the prevention of rebleeding in the setting of bleeding secondary to portal hypertension.
A case report study from Harvard Medical School, published in 1991, described three adult patients with ADHD unsuccessfully treated with traditional psychostimulant (amphetamine) therapy due to lack of effectiveness or intolerance of the psychostimulant. Nadolol was then added to the psychostimulant therapy and the combination of medications resulted in improved attention and focus with decreased medication side effects. This suggested the combination of nadolol and the psychostimulant might be effective for treatment-resistant adults with ADHD.
Patients whose heart rate is largely mediated by the sympathetic nervous system (e.g. patients with congestive heart failure or myocardial infarct) should avoid nadolol as it inhibits sympathetic function. Nadolol is also contraindicated in patients with bradycardia (slow heart rate) because of its vasodilatory effects and tendency to cause bradycardia.
Because of its beta-2 activity, nadolol causes pulmonary bronchoconstriction and should be avoided in asthma patients in preference of a beta-1 blocker. (There may be new evidence indicating that long-term non-selective beta-blocker use may actually prove to be beneficial in mild asthma.)
As nadolol, like other beta-2 blockers, inhibits the synthesis and release of glucose in response to hypoglycemia, it slows patients' recovery from acute hypoglycemic episodes and should be avoided in patients getting treatment for their diabetes mellitus. In patients with insulin-dependent diabetes, a selective beta-1 blocker is preferred over non-selective blockers.
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^ Buice RG, Subramanian VS, Duchin KL, Uko-Nne S. (1996). "Bioequivalence of a highly variable drug: an experience with nadolol". Pharmaceutical Research. 13 (7): 1109–15. doi:10.1023/A:1016031313065. PMID 8842054. ^N. Hanania, S. Singh, R. El-Wali, et al. The safety and effects of the beta-blocker, nadolol, in mild asthma: An open-label pilot study Pulmonary Pharmacology & Therapeutics, Volume 21, Issue 1, Pages 134-141