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  • Title: [Atrial natriuretic hormone in the human].
    Author: Holtz J, Münzel T, Bassenge E.
    Journal: Z Kardiol; 1987 Nov; 76(11):655-70. PubMed ID: 2962372.
    Abstract:
    The muscle cells of cardiac atria contain many secretory granula with a prohormone of 126 amino acids (ANF(1-126)). Distension of the atria causes exocytosis of the granula with cleavage of the prohormone into the hormone ANF(99-126) or alpha-ANP and the N-terminal fragment ANF(1-98) with an as yet unknown role. The plasma concentration of the hormone in normal man is in the range of 10 pM (30 pg/ml) with a plasma half-life of several minutes and a release rate of 2-3 ng/kg per minute. The plasma concentration changes in parallel with the intake of sodium chloride and is elevated acutely by all interventions which increase the blood volume, or which cause its redistribution towards the cardiopulmonary compartment. Infusions of the hormone cause diuresis and natriuresis, inhibition of the renin-angiotensin-aldosterone system and of sympathetic activity and augmentation of tissue filtration. Thus, a hormonal feedback loop for cardiac unloading by limiting the plasma volume could be assumed. However, the ANF infusion rates necessary for eliciting these actions in man induce ANF plasma concentrations above physiological levels. On the other hand, a physiological role of the hormone in this regulation is suggested by observations during long-term administration of the hormone, which demonstrate actions of the hormone at physiological plasma levels. Furthermore, experiments with injection of ANF antibodies indicate a synergistic action of ANF, together with reflexes in response to atrial distension. ANF acts by activating specific high affinity membrane receptors, resulting in intracellular cGMP formation and cGMP release into plasma and urine. These ANF receptors are "down-regulated" by infusions of the hormone and by chronic volume expansion. In fetal circulation and in congestive heart failure, there is also augmented prohormone synthesis in the cardiac ventricles, which may then contribute to the release of the hormone. Although during cardiac failure the ANF plasma levels are augmented up to 30-fold, and the atrial prohormone content is reduced, there is no indication for an exhaustion of hormone synthesis or for resetting of stimulated hormone release. In addition to its role as a peripheral hormone for "cardiac unloading", ANF occurs in the central nervous system as a neuropeptide, which might also be involved in blood pressure and volume regulation.
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