Atrial natriuretic peptide, vasopressin

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). 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

The expression of the ET-1 gene is increased by growth factors and cytokines, including transforming growth factor-B (TGF-B) and interleukin 1 (IL-1), vasoactive substances including angiotensin II and vasopressin, and mechanical stress. Expression is inhibited by nitric oxide, prostacyclin, and atrial natriuretic peptide. 

Zhou XJ, Pandian D, Wang QX, Vaziri ND (1997) Erythropoietin-induced hypertension is not mediated by alterations of plasma endothelin, vasopressin, or atrial natriuretic peptide levels. J Am Soc Nephrol 8 901-905... 

Manzanares J, Lookingland KJ, Moore KE (1990a) Atrial natriuretic peptide-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by hypothalamic tuberohypophysial or tuberoinfundibular dopaminergic neurons. Brain Res 527 103-108. 

Rosenberg GA, NavratU M, Barone F, Feuerstein G (1996a) Proteolytic cascade enzymes increase in focal cerebral ischemia in rat. J Cereb Blood Flow Metab 16 360-366 Rosenberg GA, Scremin O, Estrada E, Kyner WT (1992) Arginine vasopressin Vl-tmtagonist and atrial natriuretic peptide reduce hemorrhagic brtiin edema in rats. Stroke 23 1767-1774... 

Figure 50-12 Key elements in water homeostasis. So/id //nes indicate osmotically stimulated pathways, and dashed lines Indicate volume-stimulated pathways.The dotted lines indicate negative feedback pathways. Abbreviations ANfl atrial natriuretic peptide AVP, arginine vasopressin CNS, central nervous system C/- extracellular fluid OPR, oropharyngeal reflex. (From Reeves W,AndreoliT.The posterior pituitary and water metabolism. /n Wj7son JD, Foster DW, eds. Williams textbook of endocrinology, 8tb ed. Philadelpbia WB Sounders Co, 1992 312.)...

Badola F, Benedict C. Rapid, simplified radioimmunoassay of arginine-vasopressin and atrial natriuretic peptide in plasma. Clin Chem 1988 34 970-3. 

ACC American College of Cardiology ACE angiotensin-converting enzyme AHA American Heart Association ANP atrial natriuretic peptide ARB angiotensin receptor blocker AVP arginine vasopressin BNP B-type natriuretic peptide cAMP cyclic adenosine monophosphate CNP C-type natriuretic peptide CO cardiac output... 

FIGURE 3 Effects on the guanylate cyclase activator, atrial natriuretic peptide II (ANP II), on Ca +-dependent activation of phosphorylase a formation and intracellular Ca levels in potassium-stimulated (A and C) or vasopressin-stimulated (B and D) primary cultures of rat aortic VSMC. Cultures were incubated for one minute with the Ca +-activating stimulus in the absence or presence of different concentrations of ANP II. Asterisk denotes significance from 0 ANP II at P < 0.05. For details on the methodology, consult Corwell and Lincoln (1988). Reprinted with permission from the Journal of Pharmacol. Exp. Therap. and Williams and Wilkins, Co., Copyright 1988. 

A. Classification and Prototypes Vasoactive peptides comprise a large class of endogenous substances that function as neurotransmitters as well as local and systemic hormones. The better-known peptides include angiotensin, bradykinin, atrial natriuretic peptide, endothelin, vasoactive intestinal peptide, substance P, calcitonin gene-related peptide, vasopressin, glucagon, and several opioid peptides. Vasopressin is discussed in Chapters 15 and 37, the opioid peptides in Chapter 31, and glucagon in Chapter 41. The peptides discussed in this chapter and their effects are summarized in Table 17-1. 

Atrial natriuretic peptide (ANP) has multiple central and peripheral actions which are opposite to those induced by angiotensin II and vasopressin [69,70,128]. 

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. 

Simultaneous angiotensin I, angiotensin II, angiotensin III, atrial natriuretic peptide, bombesin, bradykinin, gonadorelin (LHRH), somatoliberin, vasopressin... 

Samson, W. K., Aguila, M. C., Martinovic, J., Antunes-Rodrigues, J., and Norris, M., Hypothalamic action of atrial natriuretic factor to inhibit vasopressin secretion. Peptides 8,449-454 (1987). 

Numerous neuroendocrine biomarkers correlate with severity of cardiac dysfunction. Heart failure is associated with increase in peripheral vascular resistance due to increases in sympathetic tone, norepinephrine, renin, angiotensin II, arginine vasopressin, and endothelin-1. The increased venous pressure causes atrial distension that stimulates production and release of atrial and brain natriuretic peptides (ANP, BNP) from the atria and ventricles, respectively. ANP inhibits the renin-angiotensin-aldosterone system. In humans and mammals, BNP has been found to be an early biomarker of left ventricular hypertrophy developing with doxorubicin cardiotoxicity, congestive heart failure, or occult dilated cardiomyopathy (Erkus et al. 2006 Walker 2006 Oyama, Sisson, and Solter 2007). 

Mental activity involves adenosine, angiotensin, atrial natriuretic factor, bombesin, bradykinin, calcitonin, calcitonin-gene related peptide (CGRP), adrenomedullin, can-nabinoid, cholecystokinin and gastrin, corticotropin-releasing factor (CRF), glutamate, histamine, melatonin, somatostatin, thyrotropin-releasing hormone, and vasopressin and oxytocin. 

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