PHSI 208 Lecture Notes - Lecture 4: Vascular Smooth Muscle, Inotrope, Pulmonary Artery
Document Summary
Contractility is controlled by the nervous and endocrine systems. Any chemical that affects contractility is called an inotropic agent, and its influence is referred to as an inotropic effect. Chemicals increasing contractility have a positive inotropic effect, and ones decreasing contractility have a negative inotropic effect. Catecholamines (norepinephrine and epinephrine) released from the sympathetic neurons or adrenal medulla cause a positive inotropic effect, regardless of edv. Contractility increases as the amount of ca2+ available for contraction increases. During action potentials, na+ enters and k+ exits. Na+ and k+ are returned to their original compartments by na-k-atpase. Ca2+ removal through ncx depends on high extracellular na+ concentrations. Cardiac glycosides (def): organic molecules obtained from certain plants (digitoxin, ouabain) containing a glycoside (sugar) that inhibits the na-k-atpase causing increased contractility. Afterload is the end load against which the heart contracts to eject blood.
