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The Renin-Angiotensin System (RAS) Zahid H. Khan, SRNA York College of Pennsylvania.
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Transcript of The Renin-Angiotensin System (RAS) Zahid H. Khan, SRNA York College of Pennsylvania.
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The Renin-Angiotensin System (RAS)
Zahid H. Khan, SRNAYork College of Pennsylvania
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DISCUSSION AGENDA
Review History of RAS
Discuss Physiology of RAS
Describe Mechanism of Action of RAS
Explain Nurse Anesthetist’s view of RAS
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SEARCH FOR THE TRUTH: 7 DECADES OF RESEARCH!
One peptide, two continents, two names
The Argentine Research Group Dr. Braun-Menendez
The United States Research Group Dr. Irvine H. Page
Linguistic confusion
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ORIGIN OF THE CLASSIC VIEW
Skeggs et al. 1956 The amino acid
sequence ANG I to ANG II
Drs. Ferreira and Silva 1965 Brazillian pit snake ACE inhibitor
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KEY ELEMENTS OF THE CLASSIC VIEW
The Juxtaglomerular Apparatus
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KEY ELEMENTS OF THE CLASSIC VIEW
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As Emerson said:
“Nothing is rich but the inexhaustible wealth of nature. She shows us only surfaces, but she is a million fathoms deep…”
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EMERGENCE OF THE CURRENT VIEW
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MECHANISM OF ACTION OF RAS
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RECEPTORS AND FUNCTIONS OF PEPTIDES
LIGAND RECEPTOR FUNCTIONS
Angiotensin II
Angiotensin III
Angiotensin II type I receptor
(AT1)
Vasoconstriction, sympathetic stimulation, aldosterone release, ADH release, fibrosis, hypertrophy, inflammation, thrombosis
Angiotensin II Angiotensin II type II receptor
(AT2)
Vasodilation, nitric oxide release, antihypertrophic, antifibrotic, antithrombotic
? Angiotensin II type III receptor Unknown
Angiotensin IV Angiotensin IV receptor Vasodilation, inflammation, improved memory, plasminogen activator inhibitor-1 release, decreased tubular sodium transport
Angiotensin (1-7) Mas receptor Inhibits cell growth. Antagonism of AT1
Renin and prorenin Renin/prorenin receptor Increased contractility, hypertrophy, fibrosis, apoptosis
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RAS: INTRACELLULAR SIGNAL TRANSDUCTION
Mitogen activated protein kinases (MAPKs) ERK P38 JNK
Transcription factors C-Jun/C-Fos ATF2
Proto-oncogene: Ras, Rac1
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RAS: INTRACELLULAR SIGNAL TRANSDUCTION
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CRNA’S VIEWPOINT
Target areas of RAS Inhibitors
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COMPARISON OF ACE INHIBITORSCharacteristic
Captopril
Enalapril
Lisinopril
Benazepril
Fosinopril
Quinapril
Ramipril
Elimination Renal Renal Renal Renal
Hepatic 50% Renal 50%
Hepatic 37%Renal 61%
Renal
Onset of hypotensive action (hr)
0.25 1 1 1 1 1 1–2
Peak hypotensive effects (hr)
1–1.5 4–6 6 2–4 2–6 2 3–6
Duration of hypotensive effects (hr)
Dose related
24 (18–30)
24 (18–30) 24 24 24 >24
(24–60)
Dose (mg)25–150, max 450
5–40, max 40
10–40, max 80
20–80, max 80
10–40, max 80
10–80, max 80
2.5–20, max 20
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COMMON ANGIOTENSIN RECEPTOR BLOCKERS
Drug Dosage
Candesartan (Atacand) 4–32 mg
Irbesartan (Avapro) 150–300 mg
Losartan (Cozaar) 50–100 mg
Telmisartan (Micardis) 40–80 mg
Valsartan (Diovan) 80–320 mg
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CRNA’S VIEWPOINT Preoperative period ACEIs OR ARBs Medication taken
before surgery? Target organ
damage?
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CRNA’S VIEWPOINT
Intra-op Management
Fluid volume management
Maintenance of arterial BP
Electrolyte abnormalities
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CRNA’S VIEWPOINT
RAS: A friend or foe
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CRNA’S VIEWPOINT
Should ACEI or ARB be held prior to surgery? “Renin-angiotensin blockade is
associated with increased mortality after vascular surgery”
“Should I continue or discontinue that medication?”
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SUMMARY
Complex and multilayered physiology Existence of
Intracellular RAS Better comprehension
= Better pharmaceutical agents
Benefits of RAS blockade
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DISCUSSION
Which is more effective, ACEI or ARBs?
Is dual blockade of RAS better? ONTARGET Study
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REFERENCES
Desborough, J. P. (2006). Physiologic responses to surgery and trauma. In H. C. Hemmings Jr& P. M. Hopkins, Foundations of Anesthesia Basic Sciences for Clinical Practice (2nd ed.) (pp. 867-874). Philadelphia: Mosby Elsevier.
Ferrario, C. M. (2010). New physiological concepts of the renin-angiotensin system from the investigation of precursors and products of angiotensin I metabolism. Hypertension, 55(Pt. 2), 445-452. doi: 10.1161/hypertensionaha.109.145839
Fyhrquist, F., & Saijonmaa, O. (2008). Renin-angiotensin system revisited. Journal of Internal Medicine, 264, 224-236. doi: 10.1111/j.1365-2796.2008.01981.x
Gradman, A. H. (2009). Evolving understanding of the renin-angiotensin-aldosterone system: Pathophysiology and targets for therapeutic intervention. American Heart Journal, 157(6, Suppl. 1), 51-56. doi: 10.1016/j.ahj.2009.04.005
Grandi, A. M., & Maresca, A. M. (2006). Blockade of the renin-angiotensin-aldosterone system: Effects on hypertensive target organ damage. Cardiovascular & Hematological Agents in Medicinal Chemistry, 4, 219-228.
Guyton, A. C., & Hall, J. E. (2006). Textbook of medical physiology (11th ed.). Philadelphia: Elsevier Saunders.
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REFERENCES
Jankowski, P., Safar, M. E., & Benetos, A. (2009). Pleiotropic effects of drugs inhibiting the renin-angiotensin-aldosterone system. Current Pharmaceutical Design, 15, 571-584.
Lee, H. T, Vidovich, M., & Mujais, S. (2006). Renal Physiology. In H. C. Hemmings Jr, & P. M. Hopkins, Foundations of Anesthesia Basic Sciences for Clinical Practice (2nd ed.) (pp.
687-698). Philadelphia: Mosby Elsevier.Mallick, A., & Bodenham, A. R. (2006). Regulation of blood volume and electrolytes. In H.
C. . Hemmings Jr & P. M. Hopkins, Foundations of Anesthesia Basic Sciences for ClinicalPractice (2nd ed.) (pp. 709-722). Philadelphia: Mosby Elsevier.
Martini, F. H., Ober, W. C., Garrison, C. W., Welch, K., & Hutchings, R. T. (2006). Fundamentals of Anatomy & Physiology (7th ed.). New York: Pearson Benjamin Cummings.
Qiagen Sample & Assays Technologies. (2011). Renin Angiotensin Pathway. Retreived from Qiagen website: https://www.qiagen.com/geneglobe/pathwayview.aspx?pathwayID=388
Skrbic, R., & Igic, R. (2009). Review: Seven decades of angiotensin (1939-2009). Peptides, 30(2009), 1945-1950. doi: 10.1016/j.peptides.2009.07.003