BIOM3010 Lecture Notes - Lecture 8: Angiotensin-Converting Enzyme, Left Ventricular Hypertrophy, Thiazide
Document Summary
Defined as chronic elevation in blood pressure. Factors increasing an already existing genetic predisposition: dietary factors, salt, obesity, alcohol, stress, lack of exercise, these go on to increase co, tpr and bp. No real sx many go undiagnosed or are inadequately controlled. Most important preventable risk factor for premature death (above smoking) Endocrine: primary (essential) 90% of cases; no underlying causes, probably genetic and lifestyle, secondary due to specific causes. Renal stenosis narrowing of blood vessel, conserves salt, increase volume, bp up. Pheochromocytoma adrenal medulla tumour that secrete catecholamines in an unregulated manner. Primary aldosteronism overproduction of aldosterone, na+ retention leads to increased plasma volume and thus bp (also decrease in renin) Raas renin-angiotensin-aldosterone-system: granular cells in the kidney secrete renin, renin converts angiotensinogen (from liver) into angiotensin 1. In lungs: angiotensin 1 is converted into angiotensin 2 by angiotensin converting enzyme: angiotensin 2 triggers the release of aldosterone (hormone) from adrenal cortex, binds to at1r receptor on heart/vasculature vasoconstriction,
