Natriuretic hormones

Nontraditional Hormones. Novel hormones identified ia cardiovascular tissue have profound effects on maintenance of blood pressure and blood volume ia mammals. Atrial natriuretic hormone (ANH) is a polypeptide hormone secreted from the atria of the heart. When the cardiac atrium is stretched by increased blood volume, secretion of ANH is stimulated ANH ia turn increases salt and water excretion and reduces blood pressure (6). Endothelin is a polypeptide hormone secreted by endothehal cells throughout the vasculature. Although endothelin is released into the circulation, it acts locally in a paracrine fashion to constrict adjacent vascular smooth muscle and increase blood pressure (7). 

L3. Laragh, J. H., Atrial natriuretic hormone, the renin-aldosterone axis, and blood pressure-electrolyte homeostasis. N. Engl. J. Med. 313, 1330-1340 (1985). 

V4. Vermes, I., Beishuizen, A., Hampsink, R. M and Haanen, C., Dissociation of plasma adreno-corticotropin and cortisol levels in critically ill patients Possible role of endothelin and atrial natriuretic hormone. J. Clin. Endocrinol. Metab. 80, 1238-1242 (1995). 

Humoral abnormalities involving the renin-angiotensin-aldosterone system, natriuretic hormone, or hyperinsulinemia ... 

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. 

Keck ME, Holsboer F (2001) Hyperactivity of CRH neiu-onal circuits as a target for therapeutic interventions in affective disorders. Peptides 22 835-844 Kellner M, Wiedemann K, Holsboer F (1992) ANF inhibits the CRH-stimulated secretion of ACTH and cortisol in man. Life Sci 50 1835-1842 Kellner M, Herzog L, Yassouridis A, Holsboer F, Wiedemann K (1995) A possible role of atrial natriuretic hormone in pituitary-adrenocortical imresponsiveness in lactate-induced panic disorder. Am J Psychiatry 152 1365-1367 Kennedy JL, Bradwein J, Koszycki D (1999) Investigation of cholecystokinin system genes in panic disorder. Mol Psychiatry 4 284-285... 

StrOhle A, Kellner M, Holsboer F, Wiedemann K (1998) Atrial natriuretic hormone decreases endocrine response to a combined dexamethasone corticotropin-releasing hormone test. Biol Psychiatry 43 371-375... 

While the angiotensins promote release of aldosterone, the atrial natriuretic hormoner aa cc inhibits release. This group of 21- to 33-residue polypeptides, secreted by cells of the atria (auricles) of the heart, also inhibits release of renin and promotes secretion of both Na+ and water. Thus, they antagonize the action of aldosterone, which promotes Na+ retention. However, there is uncertainty as to the significance of these peptides. The following metabolite of y-tocopherol (Fig. 15-24) has been isolated from urine and is proposed as a new endogenous natriuretic factor.dd... 

A major advance based on cloned genes is the production of new medicines previously unavailable or available in only small amounts. Among these are the interferons287 (Chapter 31) and many hormones such as the interleukins produced by lymphocytes448 and the atrial natriuretic hormones (Chapter 23). Another candidate is the al-protease inhibitor (Chapter 12). Perhaps better inhibitors than the natural one can be devised and produced in bacteria.449... 

Atrial natriuretic hormone (peptide) Heart Kidneys Increase Na+ excretion... 

Studies have led to evidence suggesting that two types of Na+ transport mechanisms may be defective in vascular smooth muscle cells in some forms of hypertension. These are (a) an increased cell membrane permeability to Na+, and (b) decreased active pumping of Na+ at the prevailing intracellular Na+ concentration, resulting from elevated blood levels of an endogenous inhibitor of the Na+-K+-ATPase, the so-called natriuretic hormone. The increase in intracellular Na+ concentration, in turn, promotes Ca2+ influx by the operation of the Na+/Ca2+ exchanger... 

ATRIOPEPTIN-28 (HUMAN) CARPERITIDE HORSE ATRIAL NATRIURETIC PEPTIDE-28 HUMAN ATRIAL NATRIURETIC FACTOR (99-126) a-hmn ATRIAL NATRIURETIC HORMONE HUMAN ATRIAL NATRIURETIC PEPTIDE (1-28) (99-126) HUMAN ATRIOPEPTIN(l-28) HUMAN ATRIOPEPTIN(99-126) (99-126)-hmn PROATRIOPEPTIN SUN-4936 TRIO-PEPTIN (HUMAN a-COMPONENT)... 

Several humoral abnormalities may be involved in the development of essential hypertension. These abnormalities may involve the RAAS, natriuretic hormone, and hyperinsulinemia. 

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. 

The homeostasis afforded by the kidneys is affected by catecholamines, prostaglandins, renin, antidiuretic hormone, natriuretic hormone, and the number of functioning nephrons. The intact nephron hypothesis described by Bricker," which was first published more than 30 years ago, proposes that kidney function of patients with renal disease is the net result of a reduced number of appropriately functioning nephrons. As the number of nephrons is reduced from the initial complement of 2 million, those that are unaffected compensate for those that are damaged by disease or toxic... 

The natriuretic effect of prestegane B observed in vivo [306] could have to do with the inhibition of Na+/K+-ATP activity demonstrated in vitro in previous studies. This synthetic lignan probably acts beyond the proximal tubule, as urinary phosphate was not altered. Prestegane B mimics the effects of other endogenous diuretic and natriuretic hormones, but its site of action and its effect on renal hemodynamics are obviously different. 

Diuretics are drugs that increase the rate of urine flow clinically useful diuretics also increase the rate of excretion of Na+ (natiiuresis) and an accompanying anion, usually CD. Most clinical applications of diuretics aim to reduce extracellular fluid volume by decreasing total-body NaCl content. Although continued administration of a diuretic causes a sustained net deficit in total-body Na+, the time course of natriuresis is finite because renal compensatory mechanisms bring Na+ excretion in line with Na+ intake, a phenomenon known as diuretic braking. Compensatory mechanisms include activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone axis, decreased arterial blood pressure (which reduces pressure natriuresis), hypertrophy of renal epithelial cells, increased expression of renal epithelial transporters, and perhaps alterations in natriuretic hormones such as atrial natriuretic peptide. 

Johnson, A., Lermioglu, F., Garg, U. C., Morgan-Boyd, R., and Hassid, A. (1988). A novel biological effect of atrial natriuretic hormone Inhibition of mesangial cell mitogenesis. Biochem. Biophys. Res. Commun. 152, 893-897. 

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