Summary
The syndrome of congestive heart failure is characterized not only by impaired ventricular function, but also by an increase in some endogenous substances leading to vasoconstriction as well as water and salt retention. Although activation of the systems that release these substances is presumed to be compensatory, the sympathetic nervous system and renin-angiotensin-aldosterone system may contribute to the pathogenesis of the syndrome. Opposite to the effects of these two systems are those evoked by the release of atrial natriuretic peptide which exerts a potent direct vasodilation and natriuresis. In addition, atrial natriuretic peptide inhibits the release of norepinephrine from nerve terminals and suppresses the formation of renin. However, the natriuretic and vasodilator effects of the peptide in patients with congestive heart failure are outweighed by the sodium retention and vasoconstriction caused by sympathetic stimulation and activation of the renin-angiotensin-aldosterone system. The reasons for this are not entirely known. The atrial stretch receptors that are responsible for the release of the peptide become impaired, and it has been suggested that patients with heart failure may adapt to the physiological effects of atrial natriuretic peptide.
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Ferrari, R. (1993). Neuroendocrine Response to Heart Failure. In: Ostadal, B., Dhalla, N.S. (eds) Heart Function in Health and Disease. Developments in Cardiovascular Medicine, vol 140. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3090-9_23
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DOI: https://doi.org/10.1007/978-1-4615-3090-9_23
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