IMED3001 Study Guide - Midterm Guide: Adenylyl Cyclase, Ejection Fraction, Sympathetic Nervous System
Initial stretch will increase ventricular chamber size and improve stroke volume for a given ejection fraction. Branched myocardial cells will augment contractile force upon stretch. But only up to a point. Further stretch causes (sometimes irreversible) decline in contractility. With a resultant fall in ejection fraction. Reduced vagal (parasympathetic) activity to the heart. Elevation of circulating noradrenaline increasedhr, blood vessel constriction, and positive cardiac contractility. Depletion cardiac noradrenaline down regulation of cardiac beta-adrenergic receptors. Uncoupling of cardiac proteins,reduced adenylate cyclase. Reduced metabolic activity at the cellular level,depleted. Increasing the work of the heart. Greater chance of lethal cardiac arrhythmias. Angiotensin ii then constricts blood vessels, increases the secretion of anti. Diuretic hormone (adh, vasopressin) and aldosterone, and stimulates the hypothalamus to activate the thirst reflex. These result in an increase in blood pressure: renin angiotensin aldosterone system (raas) Nacl & h2o retention, increased bp, vasoconstriction, cardiac hypertrophy, apoptosis (cell death) and fibrosis (scarring) This is a classic feedback loop.