Advertisement

Renin–Angiotensin–Aldosterone Axis Modulators and Other Vasodilators

  • Chirag Bavishi
  • Roberto Ramirez
  • Franz H. Messerli
Chapter
Part of the Contemporary Cardiology book series (CONCARD)

Abstract

The renin–angiotensin–aldosterone system (RAAS) is a hormonal loop that regulates blood pressure and fluid balance. This system plays a prominent role in the pathophysiology of cardiac diseases, especially hypertension and systolic heart failure. Aldosterone leads to local effects of vasoconstriction and sodium resorption, and potentiates inflammation and fibrosis in several organs, including the heart. Inhibitors of the RAAS, particularly angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), are commonly recommended and prescribed to patients with cardiac disease. The role of the RAAS in heart disease and the hemodynamic effects of specific inhibitors of this system will be reviewed here.

Keywords

Renin Angiotensin Aldosterone Inhibitors Hypertension Heart failure 

References

  1. 1.
    Konstam MA, Rousseau MF, Kronenberg MW, Udelson JE, Melin J, Stewart D, et al. Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dysfunction in patients with heart failure. SOLVD Investigators. Circulation. 1992;86(2):431–8.CrossRefGoogle Scholar
  2. 2.
    Lund-Johansen P, Omvik P. Cardiac effects of ACE inhibition. J Cardiovasc Pharmacol. 1993;22(Suppl 1):S36–40.CrossRefGoogle Scholar
  3. 3.
    Oren S, Messerli FH, Grossman E, Garavaglia GE, Frohlich ED. Immediate and short-term cardiovascular effects of fosinopril, a new angiotensin-converting enzyme inhibitor, in patients with essential hypertension. J Am Coll Cardiol. 1991;17(5):1183–7.CrossRefGoogle Scholar
  4. 4.
    Paulson OB, Waldemar G, Andersen AR, Barry DI, Pedersen EV, Schmidt JF, et al. Role of angiotensin in autoregulation of cerebral blood flow. Circulation. 1988;77(6 Pt 2):I55–8.PubMedGoogle Scholar
  5. 5.
    Daly P, Rouleau JL, Cousineau D, Burgess JH. Acute effects of captopril on the coronary circulation of patients with hypertension and angina. Am J Med. 1984;76(5B):111–5.CrossRefGoogle Scholar
  6. 6.
    Ting CT, Yang TM, Chen JW, Chang MS, Yin FC. Arterial hemodynamics in human hypertension. Effects of angiotensin converting enzyme inhibition. Hypertension. 1993;22(6):839–46.CrossRefGoogle Scholar
  7. 7.
    Mallareddy M, Parikh CR, Peixoto AJ. Effect of angiotensin-converting enzyme inhibitors on arterial stiffness in hypertension: systematic review and meta-analysis. J Clin Hypertens (Greenwich). 2006;8(6):398–403.CrossRefGoogle Scholar
  8. 8.
    Mathew J, Sleight P, Lonn E, Johnstone D, Pogue J, Yi Q, et al. Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor ramipril. Circulation. 2001;104(14):1615–21.CrossRefGoogle Scholar
  9. 9.
    Messerli FH, Bangalore S, Bavishi C, Rimoldi SF. Angiotensin-converting enzyme inhibitors in hypertension: to use or not to use? J Am Coll Cardiol. 2018;71(13):1474–82.CrossRefGoogle Scholar
  10. 10.
    Luther JM, Wang Z, Ma J, Makhanova N, Kim HS, Brown NJ. Endogenous aldosterone contributes to acute angiotensin II-stimulated plasminogen activator inhibitor-1 and preproendothelin-1 expression in heart but not aorta. Endocrinology. 2009;150(5):2229–36.CrossRefGoogle Scholar
  11. 11.
    Mahmud A, Mahgoub M, Hall M, Feely J. Does aldosterone-to-renin ratio predict the antihypertensive effect of the aldosterone antagonist spironolactone? Am J Hypertens. 2005;18(12. Pt 1):1631–5.CrossRefGoogle Scholar
  12. 12.
    Fraccarollo D, Galuppo P, Schraut S, Kneitz S, van Rooijen N, Ertl G, et al. Immediate mineralocorticoid receptor blockade improves myocardial infarct healing by modulation of the inflammatory response. Hypertension. 2008;51(4):905–14.CrossRefGoogle Scholar
  13. 13.
    Perrier E, Kerfant BG, Lalevee N, Bideaux P, Rossier MF, Richard S, et al. Mineralocorticoid receptor antagonism prevents the electrical remodeling that precedes cellular hypertrophy after myocardial infarction. Circulation. 2004;110(7):776–83.CrossRefGoogle Scholar
  14. 14.
    Chen Y, Meng L, Shao H, Yu F. Aliskiren vs. other antihypertensive drugs in the treatment of hypertension: a meta-analysis. Hypertens Res. 2013;36(3):252–61.CrossRefGoogle Scholar
  15. 15.
    Solomon SD, Shin SH, Shah A, Skali H, Desai A, Kober L, et al. Effect of the direct renin inhibitor aliskiren on left ventricular remodelling following myocardial infarction with systolic dysfunction. Eur Heart J. 2011;32(10):1227–34.CrossRefGoogle Scholar
  16. 16.
    Schroten NF, Damman K, Hemmelder MH, Voors AA, Navis G, Gaillard CA, et al. Effect of additive renin inhibition with aliskiren on renal blood flow in patients with Chronic Heart Failure and Renal Dysfunction (Additive Renin Inhibition with Aliskiren on renal blood flow and Neurohormonal Activation in patients with Chronic Heart Failure and Renal Dysfunction). Am Heart J. 2015;169(5):693–701 e3.CrossRefGoogle Scholar
  17. 17.
    Doulton TW, He FJ, MacGregor GA. Systematic review of combined angiotensin-converting enzyme inhibition and angiotensin receptor blockade in hypertension. Hypertension. 2005;45(5):880–6.CrossRefGoogle Scholar
  18. 18.
    Franciosa JA, Limas CJ, Guiha NH, Rodriguera E, Cohn JN. Improved left ventricular function during nitroprusside infusion in acute myocardial infarction. Lancet. 1972;1(7752):650–4.CrossRefGoogle Scholar
  19. 19.
    Guiha NH, Cohn JN, Mikulic E, Franciosa JA, Limas CJ. Treatment of refractory heart failure with infusion of nitroprusside. N Engl J Med. 1974;291(12):587–92.CrossRefGoogle Scholar
  20. 20.
    Chatterjee K, Parmley WW, Ganz W, Forrester J, Walinsky P, Crexells C, et al. Hemodynamic and metabolic responses to vasodilator therapy in acute myocardial infarction. Circulation. 1973;48(6):1183–93.CrossRefGoogle Scholar
  21. 21.
    Flaherty JT, Magee PA, Gardner TL, Potter A, MacAllister NP. Comparison of intravenous nitroglycerin and sodium nitroprusside for treatment of acute hypertension developing after coronary artery bypass surgery. Circulation. 1982;65(6):1072–7.CrossRefGoogle Scholar
  22. 22.
    Haber HL, Simek CL, Bergin JD, Sadun A, Gimple LW, Powers ER, et al. Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance. J Am Coll Cardiol. 1993;22(1):251–7.CrossRefGoogle Scholar
  23. 23.
    Massie B, Chatterjee K, Werner J, Greenberg B, Hart R, Parmley WW. Hemodynamic advantage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure. Am J Cardiol. 1977;40(5):794–801.CrossRefGoogle Scholar
  24. 24.
    Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325(5):303–10.CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Chirag Bavishi
    • 1
  • Roberto Ramirez
    • 2
  • Franz H. Messerli
    • 3
  1. 1.Department of CardiologyLifespan Cardiovascular Institute, Rhode Island Hospital, Warren Alpert Medical School of Brown UniversityProvidenceUSA
  2. 2.Department of CardiologyMount Sinai St. Luke’s HospitalNew YorkUSA
  3. 3.Department of CardiologyUniversity of BernBernSwitzerland

Personalised recommendations