The Renin-Angiotensin System is a hormonal system that helps regulate blood pressure and fluid balance in the body. In hypertension (HT), which is high blood pressure, dysregulation of the RAS can contribute to the condition.
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Similar to The Renin-Angiotensin System is a hormonal system that helps regulate blood pressure and fluid balance in the body. In hypertension (HT), which is high blood pressure, dysregulation of the RAS can contribute to the condition.
Similar to The Renin-Angiotensin System is a hormonal system that helps regulate blood pressure and fluid balance in the body. In hypertension (HT), which is high blood pressure, dysregulation of the RAS can contribute to the condition. (20)
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The Renin-Angiotensin System is a hormonal system that helps regulate blood pressure and fluid balance in the body. In hypertension (HT), which is high blood pressure, dysregulation of the RAS can contribute to the condition.
1.
2. Role in pathophysiology of
◦ HT
◦ CHF
◦ MI
◦ Diabetic Nephropathy
9. Angiotensin I- Inactive
Angiotensin II- Potent vasoconstrictor
Angiotensin II Equipotent in stimulating
Angiotensin III Aldosterone sec.
Angiotensin III 1/4th potency of ing BP vs Ang
II
1/10th potency of stimulating
Adr medulla vs Ang II
14. Bioavailability reduced by food
1. Captopril
2. Moexipril
should be adm. 1 hr before meal
With other agents, Rate of absorption is
affected but not the extent
16. Pathogenesis of Hypertension
BP= CO * PR
PR Vascular Tone
1. Role of RAAS activation:- Inc. levels of
Angiotensin II
Angiotensin II acts on AT1 receptors on blood
vessels Vasoconstriction Inc. PR
Inc. BP
18. 1. Role of ACE Inhibitors:- Dec. levels of
Angiotensin II
Dec. activation of AT1 receptors on blood vessels
Vasodilatation Dec. PR Dec. BP
2. Decreased Aldosterone
Decreased Retention of Na & H20
Dec Blood Volume
Dec. in BP
19. First line agents
Monotherapy effective in 50 % of patients
Majority of patients respond to combination
therapy with Diuretics or Beta blockers
20. Safe in : Hypertensive pts with:-
Diabetes
Asthmatics
PVD, Gout, Dyslipidemia
No : Postural hypotension
Electrolyte disturbances
Feeling of weakness
CNS effects
Prevent secondary hyperaldosteronism & K+
loss due to diuretics
21. Reverse LVH & wall to lumen ratio of blood
vessels.
No rebound hypertension
Minimum worsening of QOL
26. Angiotensin II induced Mechanism of Cardiac
Hypertrophy
A. Non-hemodynamic effects :-
Expression of Protooncogenes
Production of Growth factors
Extracellular matrix proteins
28. ACE Inhibitors & ARB`s help in reversal of
Cardiac Hypertrophy by inhibiting
Angiotensin II induced mechanisms
29. Hypotension-steep fall in BP with first dose
Patients at inc risk:-
1. Salt depleted
2. With CHF
3. On multiple Anti-hypertensives
Precautions:-
1. Start with very small doses
2. Salt intake should be increased
3. Withdraw Diuretics
30. Cough-Dry brassy cough
Incidence 5-20%
Onset b/w 1 week & 6 months after
initiation of therapy
Mechanism -Accumulation of Bradykinin
,PG`s and Substance P in lungs
On withdrawal disappears within 4 days
40. Bioavailabilty < 50 % except Irbesartan =70 %
Dosage
◦ Losartan 50 mg od
◦ Candesartan 8 mg od
◦ Irbesartan 150-300 mg od
◦ Valsartan 80-160 mg od
◦ Telmisartan 20-80 mg od
41. Combination of ACE Inhibitors with ARB`s
◦ Both ACE Is & ARBs block RAS
◦ Difference:-
Angiotensin I
Angiotensin II
No effect on
non-ACE angiotensin II
ACE
ACEIs
Block AT1 Receptors Effective on both ACE non-ACE
angiotensin II
-
ARBs
42. With combination there is complete
suppression of RAS
No additional benefit has been observed with
combination therapy in cardiovascular
disorders
Combination therapy need to be tested in
Renal disease. In one trial combination
therapy retards progression of Non- Diabetic
Renal disease to a greater extent than with
their monotherapy.
Combination therapy is more associated with
adverse effects including Hypotension,
Syncope and Renal failure
43. #s AT1 Receptors
ACEI interfere with degradation of Bradykinin
& other ACE substitutes
Inc Bradykinin levels Cough
With ARB`s Cough is rare
44. Complete inhibition of AT1 rec activation
unlike ACE-I where alternative pathway of
Angiotensin II activates AT1 rec
