Cardiac muscle thyroid hormones

Other drugs that may interact with cardiac glycosides include the following Albuterol, amphotericin B, beta-blockers, calcium, disopyramide, loop diuretics, nondepolarizing muscle relaxants, potassium-sparing diuretics, succinylcholine, sympathomimetics, thiazide diuretics, thioamines, and thyroid hormones. 

Experimental studies have documented changes in drug response caused by increases or decreases in the number of receptor sites or by alterations in the efficiency of coupling of receptors to distal effector mechanisms. In some cases, the change in receptor number is caused by other hormones for example, thyroid hormones increase both the number of 3 receptors in rat heart muscle and cardiac sensitivity to catecholamines. Similar changes probably contribute to the tachycardia of thyrotoxicosis in patients and may account for the usefulness of propranolol, a 3-adrenoceptor antagonist, in ameliorating symptoms of this disease. 

IDL) to LDL, and probably also by maintaining lipoprotein lipase activity which promotes triglyceride clearance. In liver, kidney, skeletal muscle, cardiac muscle, and adipose tissue, thyroid hormone stimulates Na", K+-ATPase gene expression and promotes thermogenesis. 

Increased metabolism, increased heat production, weight loss, protrusion of the eyes (exophthalmia), and an increase in bone and muscle turnover are the major symptoms. In addition, increased levels of thyroid hormone have detrimental effects on cardiac muscle and cardiac conduction, as well as on vascular smooth muscle function. 

Approximately 80% of patients with a GFR less than 20 to 30 mL/minute develop metabolic acidosis.38 Metabolic acidosis can increase protein catabolism and decrease albumin synthesis, which promote muscle wasting, and alter bone metabolism. Other consequences associated with metabolic acidosis in CKD include worsening cardiac disease, impaired glucose tolerance, altered growth hormone and thyroid function, and inflammation.38... 

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