Beta blockers that are cardioselective, like atenolol, mainly block the beta-1 receptors in the heart to slow the rate and force of contraction, which is good for certain heart conditions. But for someone with asthma, even selective blockers can sometimes affect the beta-2 receptors in the lungs and cause tightening—this cardioselectivity matters to minimise that risk. Yet, in my work on ADRB2 gene polymorphisms here, I see many patients with a certain genetic variant where even 'selective' blockers provoke a stronger bronchial reaction than textbooks say. My data from Pune shows we cannot rely on Western-derived drug profiles alone; our genetic landscape demands more caution.
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