Beta-blockers or beta-receptor blockers are mainly used in the treatment of heart disease, but also in hyperthyroidism, pheochromocytoma, glaucoma and as migraine prophylaxis. Structurally, beta-blockers are similar to catecholamines.
What exactly does a beta-blocker do?
Beta-receptor blockers, also called beta-blockers, are an important therapeutic pillar in the treatment of chronic heart failure. Beta-blockers are subject to prescription and must not be taken or discontinued without a doctor’s order. Also, the dosage may not be changed on its own.
But what is a beta blocker anyway? Beta-blockers lower blood pressure and the sequence of beats of the heart by inhibiting the action of the stress hormone adrenaline and the neurotransmitter and hormone norepinephrine. Blood pressure decreases and the beat rate of the heart decreases. You can find out more about the effects and side effects of beta-blockers and what to consider when taking them here.
The pharmacological classification of beta-blockers is based on their receptor affinity, β1-selectivity, partial agonistic properties, effects on other adrenergic receptors and physico-chemical properties.
Beta-blockers displace catecholamines from the β-adrenoceptors by blocking mainly β1 receptors, which are preferably located in the coronary vessels. Blockade of β1 receptors, which are normally excited by norepinephrine and adrenaline, has a negative chronotropic effect (heart rate ↓), negative dromotropic (conduction velocity ↓), negative inotropic (contractility ↓) and negative bathmotropic (excitability of the heartenz ↓).
The β1-adrenoceptor is a G-protein-coupled receptor. The agonism of the β1-adrenoceptor allows the Gs subunit to up-regulate adenylyl cyclase and convert ATP into cyclic AMP (cAMP). Elevated cAMP concentrations activate cAMP-dependent kinase A, phosphorylate calcium channels, increase intracellular calcium and calcium exchange through the sarcoplasmic reticulum, thereby increasing heartotropy. The cAMP-dependent kinase A phosphorylates the myosin light chains and thus increases the contractility of the smooth muscles. The increased contractility of the smooth muscles in the kidney in turn releases renin, which converts inactive angiotensinogen from the liver into angiotensin I, which in turn is converted into angiotensin II by the angiotensin converting enzyme (ACE), which is formed mainly in the lungs.
Due to the blockade of the receptor, a reduction in the release of angiotensin II and aldosterone also occurs as a result of the reduced renin release. Reduced angiotensin II leads to inhibition of vasoconstriction, and the reduction of aldosterone leads to inhibition of water retention.
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