PHAR 441 Lecture Notes - Lecture 14: Vasopressin Receptor 2, Tolvaptan, Antiarrhythmic Agent
10 Dec 2016
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Improve cardiac functional capacity, exercise capacity, & overall quality of life: relieve symptoms of pulmonary/peripheral congestion, prolong life expectancy, decrease progression of chf. Pharmacological therapy: diuretics, drugs that interfere with the ras system, b-blockers, vasodilators. Inhibits renal absorption of sodium renal excretion of sodium + urinary volume excretion. Ace-is moa: block ace = atii = (1) vasodilation (2) aldosterone = h2o/na retention. Continuous ace-i therapy doesn"t produce significant decreases in aldosterone because of ace escape: Cardiac and vascular chymase can also generate atii = aldosterone. Moa: blocks atii receptor at1 = atii effects without ace escape. Note we want at1 blockade, not at2 blockade (at1 = vasoconstriction, at2 = vasodilation) Spironolactone and eplerenone block aldosterone by acting on specific receptors: Kidney: (1) diuretic effect: prevent na/h2o retention = preload and afterload = edema/appearance of pulmonary and venous symptoms. (2) antiarrhythmic effect: potassium and magnesium elimination = electrolyte imbalance = cardiac arrhythmias.
