Endocrine Response to Heart Failure
Cardiac failure is a clinical entity of various causes and severity characterized by an inability of the heart to deliver a sufficient amount of blood to meet the metabolic demands of the body at rest or during exercise. Thus, as acute or chronic heart failure develops, several compensatory mechanisms are activated to maintain an adequate perfusion to vital organs such as the brain and the heart, at the expense of other non-essential organs such as the kidneys, the gut or the muscles. The neurohumoral systems involved in the maintenance of blood pressure when heart function is failing are the same as those implicated in the regulation of blood pressure when dehydration or severe losses of blood volume occur i.e. the sympathetic nervous system, the renin-angiotensin-aldosterone system and plasma arginine vasopressin. This endocrine response results in various degrees of peripheral vasoconstriction and renal sodium retention depending on the severity of the cardiocirculatory imbalance. In advanced heart failure, however, the increase in peripheral resistance and the enhanced sodium reabsorption with subsequent volume expansion are likely to compromise myocardial function by increasing afterload as well as myocardial oxygen consumption. A vicious circle is established that will lead to further irreversible myocardial damage despite the activation of other systems with vasodilatory and natriuretic properties such as the atrial natriuretic peptide or the protaglandins. An integrated scheme demonstrating the neurohumoral consequences of heart failure is presented in Fig. 1.
KeywordsHeart Failure Congestive Heart Failure Sympathetic Nervous System Atrial Natriuretic Peptide Plasma Renin Activity
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- 1.Di Bona GF (1977) Neurogenic regulation of renal tubular sodium reabsorption. Am J Physiol 233: 173–181Google Scholar
- 4.Levine TB, Francis GS, Goldsmith SR, Simon AB, Cohn JN (1982) Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relationship to hemodynamic abnormalities in congestive heart failure. Am J Cardiol 49: 1659–1666PubMedCrossRefGoogle Scholar
- 10.Chidsey CA, Braunwald E, Morrow AG, Mason DT (1963) Myocardial norepinephrine concentration in man: Effects of reserpine and of congestive heart failure. N Engl J Med 269: 653–658Google Scholar
- 26.Deboben A, Inagami T, Ganten D (1983) Tissue renin. In: Genest J, Kuchel O, Hamet P, Cantin M (eds) Hypertension–physiopathology and treatment. McGraw-Hill, New York, pp 194–209Google Scholar
- 31.The Consensus Trial Study Group (1987) Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 23: 1429–1435Google Scholar
- 32.Fyhrquist F, Hortling L, Forslund T, Laasonen L (1982) Reduction of plasma vasopressin and renin substrate in congestive heart failure during captopril treatment. From principle to practice, Biomedical Information Co, New York pp 51–62Google Scholar
- 42.Goy JJ, Waeber B, Nussberger J, et al (1988) Infusion of atrial natriuretic peptide to patients with congestive heart failure. J Cardiovasc Pharmacol (In press)Google Scholar
- 45.Dzau VJ, Packer M, Lilly LS, Swartz SL, Hollenberg NK, Williams GH (1984) Prostaglandins in severe congestive heart failure. Relation to activation of the renin-angiotensin system and hyponatremia. N Engl J Med 310: 347–352Google Scholar
- 48.Waeber B, Aubert JF, Corder R, et al (1988) Cardiovascular effects of neuropeptide Y. Am J Hypertension (In press)Google Scholar
- 49.Lee WH, Packer M (1986) Congestive heart failure: Prognostic importance of serum sodium concentration and its modification by converting enzyme inhibition in patients with severe chronic heart failure. Circulation 73: 257–267Google Scholar