Sodium natriuretic hormones

A high sodium intake and increased circulating natriuretic hormone inhibition of intracellular sodium transport, resulting in increased vascular reactivity and a rise in BP and / Increased intracellular concentration of calcium, leading to altered vascular smooth muscle function and increased peripheral vascular resistance. 

Physiologists had postulated for a long time about the existence of a sodium excreting hormone to prevent Na overload and consequent deleterious effects of high blood pressure on the heart and vascular system. At least two such natriuretic factors have been described atrial or A-type and brain or B-type natriuretic factors. Structurally, the natriuretic factors are peptides with a cysteine-cysteine disulfide bridge creating a characteristic loop , this is illustrated by Figure 8.8. 

Natriuretic hormone inhibits sodium and potassium ATPase and thus interferes with sodium transport across ceU membranes. Inherited defects in the kidney s ability to eliminate sodium can cause an increased blood volume. A compensatory increase in the concentration of circulating natriuretic hormone theoretically could increase urinary excretion of sodium and water. However, this same hormone is also thought to block the active transport of sodium out of arteriolar smooth muscle cells. The increased intracellular concentration of sodium ultimately would increase vascular tone and BP. 

Epidemiologic and clinical data have associated excess sodium intake with hypertension. Population-based studies indicate that high-salt diets are associated with a high prevalence of stroke and hypertension. Conversely, low-salt diets are associated with a low prevalence of hypertension. Clinical studies have shown consistently that dietary sodium restriction lowers BP in many (but not all) patients with elevated BP. The exact mechanisms by which excess sodium leads to hypertension are not known. However, they may be linked to increased circulating natriuretic hormone, which would inhibit intracellular sodium transport, causing increased vascular reactivity and increased BP. 

Inasmuch as sodium intake may vary considerably, the maintenance of sodium homeostasis requires a broadly adjustable mechanism of renal sodium excretion and reabsorption. Regulatory mechanisms for sodium reabsorption in the kidney include (1) rapid adjustment of the levels of tubular reabsorption through the glomerular filtration rate (2) secretion of aldosterone, which stimulates sodium reabsorption (3) the possible elaboration of a natriuretic hormone that stimulates secretion. 

At least three other groups of factors believed to regulate sodium secretion are neurogenic factors, switches from salt-conserving to salt-wasting nephrons, and natriuretic hormones. When dietary sodium is low, renal excretion decreases within 4 days to levels approaching zero. Reduced renal excretion results in part from aldosterone production. However, a decrease in urinary sodium has been observed with normal levels of aldosterone secretion. Consequently,... 

In reviewing the various hypotheses about regulation of sodium metabolism. Mills [28] proposed that renal sodium excretion depends on a pressure-sensitive mechanism near the juxtaglomerular cells that releases an active natriuretic hormone promptly when the site is stimulated by an increase in pressure. Conversely, sodium retention is believed to be caused by a decrease in this substance, by a fall in glomerular filtration rate, and by the release of renin to increased aldosterone production [29, 30]. 

Although many laboratories have attempted to demonstrate the existence of a natriuretic hormone, the most conclusive evidence in support of its existence was obtained in an isolated perfused dog kidney with blood of expanded dogs. A decrease in tubular sodium reabsorption was demonstrated [31], even when renal blood flow was reduced and in the absence of renal vasodilation. 

Nevertheless, claims of partial purification of the natriuretic hormone are not definitive. Moreover, well-known hormones, such as calcitonin and a-NSH, could also be responsible for the natriuretic effect. It is questionable that either of these hormones plays a considerable role in regulating sodium metabolism. Hormone responses to sodium loads and losses are summarized in Fig. 9-9, and the hypothetical role of the natriuretic hormone is illustrated in Fig. 9-10. 

Hypernatremia is not an absolute finding in primary hyperaldosteronism, and a mechanism of renal adaptation has been proposed. Thus, in progressive aldosteronism, salt retention activates a nonaldoste-ronic mechanism of sodium regulation, which increases sodium excretion in the distal tubules without affecting the proximal tubule, thus reestablishing the balance between sodium intake and excretion. Whether the postulated natriuretic hormone [32] is involved remains to be seen (see Fig. 9-12). 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Atrial natriuretic peptides (ANP) a hormone that is released by cardiac cells following a high blood pressure. It is involved in the control of water, sodium and adiposity. It is also known as atrial natriuretic factor (ANF) and atriopeptin. 

Renal epithefial cell membranes also contain proteins that act as ion channels. For example, there is one for sodium that is closed by amiloride and modulated by hormones such as atrial natriuretic peptide (ANP). Ion channels enable much... 

Atrial natriuretic peptide Atrial natriuretic peptide is a polypeptide hormone predominantly secreted by the cardiocytes of the right atrium of the heart. It increases urinary. sodium excretion. The physiological role, if any, of this hormone is unclear, but it probably only plays a minor role in the regulation of ECF volume and sodium concentration. To date no disease slate can be attributed to a primary disorder in the secretion of atrial natriuretic peptide. 

Sodium (Na ) Aldosterone Antidiuretic hormone (ADH)—water regulation Atrial natriuretic peptide (ANP) Renal reabsorption Renal excretion... 

In the distal portion of the nephron (sodium) and collecting ducts (water), reabsorption is facultative, dependent on body needs and secondary to hormonal stimulation (aldosterone for sodium and antidiuretic hormone (ADH, vasopressin) for water). The atrial natriuretic peptide (ANP) also plays a role by decreasing sodium reabsorption. 

---