Revised: November 29, 2013
Accepted: December 17, 2013
Published online: January 26, 2014
The discovery of the natriuretic peptide system in the early 1980s aroused great interest among clinical cardiologists. The heart was not a mechanical pump alone, but also an endocrine organ that had powerful effects on blood circulation. Natriuretic peptides caused both natriuresis and diuresis, and they responded to a volume overload which caused either stretch or pressure on the heart. As a result, the findings led to the conclusion that the human body had a hormone with effects similar to those of a drug which treats high blood pressure. Later, it became evident that the volume contraction was fortified by extrarenal plasma shift. Here, a hypothesis is presented in which the role of natriuretic peptides is to regulate oxygen transport as the volume contraction leads to hemoconcentration with an increased oxygen-carrying capacity. Wall stress, either chemical or mechanical, changes the oxygen gradient of the myocardium and affects the diffusion of oxygen within a myocyte. In support of this hypothesis, hypoxia-response elements have been found in both the atrial natriuretic peptide and the brain natriuretic peptide genes.
Core tip: A new concept is suggested for the understanding of the physiology of natriuretic peptides. Both chemical and physical challenges will ultimately increase the oxygen consumption of the heart which is the factor regulating the release of natriuretic peptides. Diuresis, natriuresis and plasma shift lead to hemoconcentration and the oxygen transport in human body will be enhanced.