Hormonal regulation plays an important role in the long-term control of blood pr

The hormones responsible for long-term regulation of blood pressure include angiotensin II, aldosterone, atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and erythropoietin. The regulation of angiotensin II and aldosterone are interrelated. The pathway to aldosterone release starts with renin. This enzyme is released from granular cells of the macula densa in response to 1) a decrease in afferent arteriole pressure, 2) a decrease in filtrate sodium and chloride in the distal tubule, and 3) an increase in renal sympathetic activity originated by activation of the baroreflex. Renin converts angiotensinogen into angiotensin I. Thereafter, angiotensin converting enzyme (located on pulmonary capillary endothelial cells) converts angiotensin I into angiotensin II, which stimulates the release of aldosterone. Aldosterone affects principal cells of the late distal tubule and collecting ducts by increasing the number and open sodium channels in the apical membrane and increasing the number of Na+/K+ pumps in the basolateral membrane. This results in an increased reabsorption of sodium. In addition, angiotensin II affects blood pressure by 1) its vasoconstrictive properties, 2) altering thirst at the hypothalamus, and 3) stimulating ADH release. ANP is counterregulatory to aldosterone and is released in response to stretch of the atria (increased blood pressure). Once released, ANP decreases glomerular filtration rate by decreasing glomerular capillary pressure through concomitant dilation of the afferent arteriole and constriction of the efferent arteriole. In addition, ANP decreases the number of open sodium channels in the apical membrane and decreases the release of ADH. The primary stimulation for the release of ADH is an increase in osmolarity within the hypothalamus. Secondarily, the release of ADH is modified by angiotensin II (increased) and ANP (decreased). ADH increases blood pressure by altering the reabsorption of water. This occurs through the insertion of aquaporin-2 into the membrane of cells within the collecting ducts. ADH also increases the number of sodium channels in the apical membrane of principal cells. Finally, erythropoietin is stimulated by a decrease in blood flow to the kidneys, which induces a hypoxia within the kidneys. Since erythrocytes make up about 45% of the volume of blood, any changes in their production will affect blood volume.