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Sumario Vol. 42 - Nº 1 Enero - Marzo 2013

Natriuretic Peptides: the missing link of the cardiometabolic physiology?

Hugo Ramos.

Cátedra de Medicina II.
Universidad Nacional de Córdoba.
Córdoba. Argentina.
Comité de Cardiopatía Isquémica de la Federación Argentina de Cardiología. Av. Caraffa 2349 X5008 KKF
Córdoba. República Argentina.
E Mail

Los editoriales representan la opinión de los autores,
no necesariamente las del Comité Editorial de la Revista FAC.
Rev Fed Arg Cardiol. 2013; 42(1): 3-4


Print version Imprimir sólo la columna central

 

“The Origin of Species” by Darwin was one of the bases to understand the adaptation mechanisms of living beings and subsequently, the discoveries of physiology got us closer to the molecular mechanisms through which they occur. In this regard, sea living beings, after successive adaptations became terrestrial, they carry plasma in their vascular system, the chemical composition of which resembles that of the sea, from where they come. To regulate the composition of plasma, some species like mammals for instance, use Natriuretic Peptides (NPs), cardiac hormones that have multiple functions and that currently work as clinical markers in heart failure, acute coronary syndromes, sepsis, and acute rejection of cardiac transplant. Until its discovery, there were “black holes” that did not allow us to understand some of the mechanisms that linked the cardiac and renal physiology, but once figured out, the veil fell and basic and clinical researchers could solve concrete problems and come up with new questions. Although clinical bibliography has disseminated that the Atrial Natriuretic Factor (ANF), also called Atrial Natriuretic Peptide (ANP) is secreted by the atria and the Brain Natriuretic Peptide (BNP) by the ventricles, there are enough data to support that the main source for both hormones are the atria. It has been proven that the messenger ribonucleic acid (mRNA) of ANP and BNP are much more abundant in the atrial than in the ventricular tissue; besides, the concentrations of C-terminal tails of ANP and BNP (CT-ANP and CT-BNP) in the hearts of rats, are significantly higher in the atria than in the ventricles, and the concentration of ANP is greater than that of BNP. In certain pathological conditions, the relative concentration of BNP is greater than that of ANP, but this should not modify the concept that in the atria, the ventricles and in blood the concentration of ANP is greater than that of BNP [1,2]. This anatomo-functional datum could be quite significant, since although ANP and BNP share similar functions, some others are differentiated. For example, in conditions of hemodynamic overload of the left ventricle, the blood levels of both hormones increase, but if inflammation predominates, as in sepsis or myocarditis, the increase of BNP is far above that of ANP. The only situations in which BNP increases above ANP are the acute rejection of cardiac transplant and the exposition of myocardial cells to inflammatory cytokines [3,4]. That is to say, NPs are also secreted before metabolic and inflammatory signs and not just mechanical ones.

Recently, a great interest has developed on the relation NPs have with obesity, metabolic syndrome and type 2 diabetes mellitus, since it has been verified that the plasma levels of NPs are inversely proportional to the body mass index, both in healthy people and in those suffering heart failure. Since there is an interaction between NPs and some intestinal peptides, it is possible that there is an intestine-brain-heart axis. For instance, ghrelin, a peptide produced by the fundic cells of the stomach and epsilon cells of the pancreas, has a stimulant effect on appetite, sending signals to the brain to increase the ingestion of food; besides, it has vasodilator effects, stimulant of the cardiac function and memory; it is antiapoptotic of the intestinal cells and anti-inflammatory. It has been verified that the IV administration of BNP to healthy individuals significantly decreases the blood levels of ghrelin and consequently, decreases the feeling of hunger and increases the feeling of being satiated, even without having received food, without increasing the plasma levels of the anorexigenic intestinal hormone PYY [5]. In patients with heart failure, the levels of ghrelin are increased, but also those of BNP, so it is believed that due to the high levels of BNP it is not possible for ghrelin to increase more and it could be one of the causes for a decrease in appetite and cardiac cachexia. On the other hand, since the NPs receptors are widely distributed in the central nervous system, it cannot be ruled out that by direct effect, these may also act in the same way to reduce appetite [5,6]. See the paper published in pages

In this issue, Castro Torres and Fleites Pérez review the physiologic and clinical relevance that understanding the complex mechanism in which NPs are involved may have; i.e. beyond the known functions on the cardiovascular system [7]. The fact that NPs interact with intestinal peptides, with products of the adipocytes such as adiponectin and leptin, interleukins, the renin-angiotensin-aldosterone system and, possibly have direct effects on the central nervous system receptors, suggests that these cardiac hormones do not just have a function that depends on mechanical stimuli, such as the “stretching-secretion” phenomenon, but that they are a significant part of a highly specialized physiological mechanism. Currently, studies are being developed to understand better the physiology of NPs related to hypertension, obesity, type 2 diabetes, and also its therapeutic application in these pathologies [8]. So, it is possible that by revealing the functions and interactions of NPs, still not well known completely, we may find the “missing link” connecting cardiovascular physiology with the metabolism of nutrients and inflammation.

 

REFERENCES.

  1. Yokota N, Bruneau BG, Fernandez BE, et al. Dissociation of cardiac hypertrophy, myosin heavy chain isoform expression, and natriuretic peptide production in DOCA-salt rats. Am J Hypertens 1995; 8: 301-310.
  2. Ramos H, de Bold AJ. Gene expression, processing, and secretion of natriuretic peptides: physiologic and diagnostic implications. Heart Fail Clin 2006; 2: 255-268.
  3. Masters RG, Davies RA, Veinot JP, et al. Discoordinate modulation of natriuretic peptides during acute cardiac allograft rejection in humans. Circulation 1999; 100: 287-291.
  4. Ma KK, Ogawa T, de Bold AJ. Selective upregulation of cardiac brain natriuretic peptides at the transcriptional levels by proinflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38MAP kinase. J Mol Cell Cardiol 2004; 36: 505-513.
  5. Vila G, Grimm G, Resl M, et al. B-Type Natriuretic Peptide modulates ghrelin, hunger, and satiety in healthy men. Diabetes 2012; 61:2592-2596.
  6. Cao LH, Yang XL. Natriuretic peptides and their receptors in the central nervous system. Prog Neurobiol 2008; 84: 234-248.
  7. Castro Torres Y, Fleites Pérez A. Péptidos natriuréticos y obesidad. Un acercamiento a un tópico de interés. Rev Fed Arg Cardiol 2013; 42 (1) __-__.
  8. de Bold MK, Sheffield WP, Martinuk A, et al. Characterization of a long-acting recombinant human serum albumin-atrial natriuretic factor (ANF) expressed in Pichia pastoris. Regul Pep 2012; 175 (1-3): 7-10. doi: 10.1016/j.regpep.2012.01.005.
  9. de Bold AJ. A treinta años del descubrimiento del factor natriurético atrial. Rev Fed Arg Cardiol 2011; 40 (2): 102-104.

 

 

Publication: March 2013

 
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