RAS system acts to maximise glomerular filtration pressure Vasoconstriction: Systemic and (efferent>afferent arterioles) – Proximal sodium resorption (ATII) – Distal sodium resorption (aldosterone) – Water resorption and thirst (ADH) – blockers (usually end in --‐olol) • β Renin release is increased by sympathetic stimulation – Renin inhibitor (Aliskiren) • cleavage of angiotensinogen by renin Angiotensin Converting Enzyme Inhibitors (ACEIs) • End in – “--‐pril” Block production of angiotensin II – Also inhibit breakdown of bradykinin (dry cough; bradykinin sensitises pulmonary – receptors) Angiotensin II receptor blockers • End in – “--‐sartan” vasoconstriction and release of aldosterone/ADH – Spironolactone • Antagonises aldosterone – downstream of RAS –ie When to block RAS Hypertension from any cause • Heart failure • Intrinsic renal disease (PROTEINURIA) • Commonly associated with intraglomerular hypertension – All proteinuric patients should be on ACEI/ARB unless contraindicated – Renovascular disease (~ renal artery stenosis: but don’t use ACEi) • When NOT to RAS illness/haemodynamic stress • GFR critically dependent on RAS when haemodynamics are compromised (ie – w after heavy bleed etc) RAS Blockade will reduce GFR by up to 15% • If renal function very poor RAS blockade can precipitate need for dialysis – Hyperkalaemia • Reduced aldosterone will impair K+ excretion – Persistent cough with ACEI --‐> ARB •
RAS system acts to maximise glomerular filtration pressure – Vasoconstriction: Systemic and (efferent>afferent arterioles) – Proximal sodium resorption (ATII) – Distal sodium resorption (aldosterone) – Water resorption and thirst (ADH) • β blockers (usually end in --‐olol) – Renin release is increased by sympathetic stimulation • Renin inhibitor (Aliskiren) cleavage of angiotensinogen by renin • Angiotensin Converting Enzyme Inhibitors (ACEIs) – End in “--‐pril” – Block production of angiotensin II – Also inhibit breakdown of bradykinin (dry cough; bradykinin sensitises pulmonary receptors) • Angiotensin II receptor blockers – End in “--‐sartan” – vasoconstriction and release of aldosterone/ADH • Spironolactone – Antagonises aldosterone –ie downstream of RAS When to block RAS • Hypertension from any cause • Heart failure • Intrinsic renal disease (PROTEINURIA) – Commonly associated with intraglomerular hypertension – All proteinuric patients should be on ACEI/ARB unless contraindicated • Renovascular disease (~ renal artery stenosis: but don’t use ACEi) When NOT to RAS • illness/haemodynamic stress – GFR critically dependent on RAS when haemodynamics are compromised (ie w after heavy bleed etc) • RAS Blockade will reduce GFR by up to 15% – If renal function very poor RAS blockade can precipitate need for dialysis • Hyperkalaemia – Reduced aldosterone will impair K+ excretion • Persistent cough with ACEI --‐> ARB
Renal-notes-BETA.docx