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Beta-blockers act as competitive antagonists that block the effects of catecholamines at beta-adrenergic receptor sites, resulting in reduced rate and force of contraction of the heart, as well as reduced peripheral vascular resistance. [14] Non-selective beta-blockers: propranolol, nadolol, timolol; Beta-1-selective beta-blockers: atenolol ...
Beta blockers exert their pharmacological effect, decreased heart rate, by binding to and competitively antagonising a type of receptor called beta adrenoceptors. [1]In pharmacology, the term mechanism of action (MOA) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect. [2]
The combination of beta blockers and antihypertensive drugs will work on different mechanism to lower blood pressure. [17] For example, the co-administration of beta-1 blocker atenolol and ACE inhibitor lisinopril could produce a 50% larger reduction in blood pressure than using either drug alone.
Beta blockers are used to treat acute cardiovascular toxicity (e.g. in overdose) caused by sympathomimetics, for instance caused by amphetamine, methamphetamine, cocaine, ephedrine, and other drugs. [38] Combined α 1 and beta blockers like labetalol and carvedilol may be more favorable for such purposes due to the possibility of "unopposed α ...
Insulin binds to insulin receptors to decrease blood glucose levels, whilst glucagon binds to glucagon receptors to increase blood glucose levels. In cases of insulin-induced hypoglycaemia, glucagon injection could help increase blood glucose levels. [8] Another example is epinephrine (a bronchodilator) and histamine (a bronchoconstrictor).
In states of insulin resistance, beta cells in the pancreas increase their production of insulin. This causes high blood insulin (hyperinsulinemia) to compensate for the high blood glucose. During this compensated phase of insulin resistance, beta cell function is upregulated, insulin levels are higher, and blood glucose levels are still ...
Insulin is given in μU/mL. [7] Glucose and insulin are both during fasting. [2] This model correlated well with estimates using the euglycemic clamp method (r = 0.88). [2] The authors have tested HOMA and HOMA2 extensively against other measures of insulin resistance (or its reciprocal, insulin sensitivity) and β-cell function. [4] [8] [9]
Thus a lowering of disposition index predicts the conversion of insulin resistance to diabetes mellitus type 2. [13] Disposition index, but not insulin resistance, can predict type 2 diabetes in persons with normal blood glucose levels, but who do not have a family history ( genetic predisposition ) to type 2 diabetes.