Advertisement

The Renin-Angiotensin-Aldosterone System and the Sympathetic Nervous System in Congestive Heart Failure: Mutual Interactions Between Both Systems

  • P. A. van Zwieten

Abstract

Congestive heart failure is frequently accompanied by complex compensatory mechanisms, involving, among others, the peripheral sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). In many cases the reflex stimulation of these mechanisms is detrimental in the long term, although initially such mechanisms may be at least of symptomatic benefit to the patient. A renewed interest in the reflex compensation mechanisms has developed upon introduction of inhibitors of the angiotensin-converting enzyme (ACE) inhibitors captopril and enalapril in the treatment of congestive heart failure. The major therapeutic activity of ACE inhibitors is undoubtedly based upon vasodilatation and, hence, unloading of the heart. However, it could be imagined that an additional action of such drugs on the aforementioned reflex mechanism somehow contributes to the symptomatic improvement of the syndrome of congestive heart failure. This situation is made even more complex by the obvious interaction between the sympathetic nervous system (SNS) and the RAAS, the two major systems involved in the sequelae of congestive heart failure and its therapy with ACE inhibitors. Before discussing this interaction, it would seem useful to briefly review the pathophysiological changes induced by congestive heart failure in each system separately.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Antonaccio MJ, Kerwin MS (1981) Pre- und postjunctional inhibition of vascular sympathetic function by captopril in SHR; implication of vascular angiotensin II in hypertension and antihypertensive action of captopril. Hypertension 3 [Suppl 1]: 154–162Google Scholar
  2. 2.
    Bristow MR (1984) Myocardial ß-adrenergic receptor down-regulation in heart failure. Int J Cardiol 5: 648–652PubMedCrossRefGoogle Scholar
  3. 3.
    Bristow MR, Ginsburg R, Minobe W et al. (1982) Decreased catecholamine sensitivity and ß-adrenergic receptor density in failing human hearts. N Engl J Med 307: 205–211PubMedCrossRefGoogle Scholar
  4. 4.
    Cohn JN, Levine TB, Olivari MT et al. (1984) Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med 311: 819–823PubMedCrossRefGoogle Scholar
  5. 5.
    de Jonge A, Wilffert B, Kalkman HO et al. (1981) Captopril impairs the vascular smooth muscle contraction mediated by postsynaptic α 2-adrenoceptors in the pithed rat. Eur J Pharmacol 74: 385–386PubMedCrossRefGoogle Scholar
  6. 6.
    de Jonge A, Knape JTA, Van Meel JCA et al. (1983) Effect of captopril on sympathetic neurotransmission in pithed normotensive rats. Eur J Pharmacol 88: 231–249PubMedCrossRefGoogle Scholar
  7. 7.
    de Jonge A, Thoolen MJMC, Timmermans PBMWM, Van Zwieten PA (1984) Interaction of angiotensin-converting enzyme inhibitors with the sympathetic nervous system. Progr Pharmacol 5: 25–38Google Scholar
  8. 8.
    Editorial (1984) The adrenergic nervous system in heart failure. N Engl J Med 311: 850–851Google Scholar
  9. 9.
    Hatton R, Clough DP (1982) Captopril interferes with neurogenic constriction in the pithed rat by angiotensin-dependent mechanisms. J Cardiovasc Pharmacol 4: 116–123PubMedCrossRefGoogle Scholar
  10. 10.
    Knape JTA (1985) Cardiovascular actions of angiotensin II in the pithed normotensive rat. Naunyn Schmiedebergs Arch Pharmacol 329: R248Google Scholar
  11. 11.
    Langer SZ, Massingham R, Shepperson NB (1980) Presence of postsynaptic α 2-adrenoceptors of predominantly extrasynaptic location in the vascular smooth muscle of the dog hind limb. Clin Sci 59: 225S-228SPubMedGoogle Scholar
  12. 12.
    Richer C, Doussau MP, Giudicelli JF (1984) Influence of captopril and enalapril on regional vascular α-adrenergic receptor reactivity in SHR. Hypertension 6: 666–674PubMedGoogle Scholar
  13. 13.
    Romankiewicz JA, Brogden RN, Heel RC, Speight TM, Avery GS (1983) Captopril: an update review of its pharmacological properties and therapeutic efficacy in congestive heart failure. Drugs 25: 6–40PubMedCrossRefGoogle Scholar
  14. 14.
    Rona G, Chappel G, Balasz T, Goudry R (1959) An infarct-like myocardial lesion and other toxic manifestations produced by isoproterenol in the rat. Arch Pathol 67: 443–455Google Scholar
  15. 15.
    Schümann HG, Güther W (1967) Untersuchungen zum Wirkungsmechanismus von Angiotensin am isolierten Aortenpräparat und am Blutdruck von Ratten und Meerschweinchen. Naunyn Schmiedebergs Arch Pharmak Exp Path 256: 169–182CrossRefGoogle Scholar
  16. 16.
    Schümann HJ, Wagner J, Knorr A et al. (1978) Demonstration in human atrial preparations of a-adrenoceptors mediating positive inotropic effects. Naunyn Schmiedebergs Arch Pharmacol 302: 333–336PubMedCrossRefGoogle Scholar
  17. 17.
    Taher MS, McCain LG, McDonald KM, Schreier RW (1976) Effect of β-adrenergic blockade on renin response to renal nerve stimulation. J Clin Invest 57: 43–59CrossRefGoogle Scholar
  18. 18.
    Thames MD (1984) Renin release: reflex control and adrenergic mechanisms. J Hypertension 2 [Suppl 1]: 57–66Google Scholar
  19. 19.
    van Zwieten PA, Timmermans PBMWM (1984) Central and peripheral α-adrenoceptors. Pharmacological aspects and clinical potential. Adv Drug Res 13: 209–254Google Scholar
  20. 20.
    Wilffert B, Timmermans PBMWM, Van Zwieten PA (1982) Extrasynaptic location of α 2 and non-innervated β 2 adrenoceptors in the vascular system of the pithed normorensive rat.Google Scholar
  21. 21.
    Zimmerman BG (1981) Adrenergic facilitation by angiotensin: does it serve a physiological function? Clin Sci 60: 343–348PubMedGoogle Scholar
  22. 22.
    Zimmerman BG, Sybertz EJ, Wong PC (1984) Interaction between sympathetic and renin- angiotensin system. J Hypertension 2: 581–587CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

  • P. A. van Zwieten
    • 1
  1. 1.Afd. FarmacotherapieUniversiteit van AmsterdamAmsterdamThe Netherlands

Personalised recommendations