Atrial natriuretic peptide, a hormone discovered in 1981, is released from muscle cells in the atria when the atrial walls are stretched. This hormone causes the vasodilation of afferent arterioles that lead into the glomerulus and efferent arterioles that lead
out of the glomerulus, resulting in an increased glomerular filtration rate (GFR). Atrial natriuretic peptide also inhibits aldosterone secretion and sodium reabsorption from the collecting tubules. All these actions result in increased urine production and reduced blood volume.

The hormone erythropoietin (released by the kidneys) stimulates the bone marrow to produce red blood cells in response to hypoxia from conditions such as anemia or from cardiac and/or pulmonary disease. If iron stores are adequate, an increase in red blood cells results in added oxygen-carrying capacity and reduced tissue hypoxia. As renal insufficiency progresses to renal failure, the kidneys’ ability to produce erythropoietin declines, causing anemia.