BMS 420 Lecture Notes - Cyclic Adenosine Monophosphate, Myocyte, Blood Pressure
Document Summary
Increase preload higher velocity of shortening for given afterload. Isometric contraction when velocity = 0 (high afterload) Vmax is velocity of shortening at theoretical 0 load. Increased circulating epinephrine heart rate, contractility. Increased sympathetic nerve activity or decreased parasympathetic nerve activity heart rate, contractility. Increased ventricular end-diastolic volume (frank-starling law) stroke volume. Increased heart rate/increased stroke volume cardiac output. Phosphorylation of l-type ca++ channels via gs protein enhances permeability to ca++ (due to activation of adrenergic receptors by epi/ne). Enhance ca++ release by sr following receptor activation. Enhance binding to tn-c with ca++. (h+ diminishes inotropy by affinity). Calcium uptake by sr by the serca pump with phosphorylation of phospholamban. Regulation of ca++ efflux from myocyte via na+/ca++ exchange pump and atp-dependent. Glycosides inhibit na+/k+ - atpase which increases intracellular na+. Increased ca++ availability to muscle cells increases contractility. Rap (right atrial pressure) determines the extent of ventricular filling.
