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Involvement of the atrial natriuretic peptide in cardiovascular pathophysiology and its relationship with exercise

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      In this minireview we describe the involvement of the atrial natriuretic peptide (ANP) in cardiovascular pathophysiology and exercise. The ANP has a broad homeostatic role and exerts complex effects on the cardio-circulatory hemodynamics, it is produced by the left atrium and has a key role in regulating sodium and water balance in mammals and humans. The dominant stimulus for its release is atrial wall tension, commonly caused by exercise. The ANP is involved in the process of lipolysis through a cGMP signaling pathway and, as a consequence, reducing blood pressure by decreasing the sensitivity of vascular smooth muscle to the action of vasoconstrictors and regulate fluid balance. The increase of this hormone is associated with better survival in patients with chronic heart failure (CHF). This minireview provides new evidence based on recent studies related to the beneficial effects of exercise in patients with cardiovascular disease, focusing on the ANP.

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      Atrial natriuretic peptide contributes to physiological control of lipid mobilization in humans.

      In humans, lipid mobilization is considered to depend mainly on sympathetic nervous system activation and catecholamine action. A contribution of ANP was hypothesized because we have previously shown that atrial natriuretic peptide (ANP) is a lipolytic agent on isolated human fat cells. Control of lipid-mobilizing mechanisms was investigated using in situ microdialysis in subcutaneous adipose tissue (SCAT) in healthy young men during two successive exercise bouts performed at 35% and 60% peak oxygen consumption (VO2max) after placebo or acute oral tertatolol (nonselective beta-antagonist) treatment. In placebo-treated subjects, infusion of propranolol in the probe (100 micromol/l) only partially reduced (40%) the increment in extracellular glycerol concentration (EGC) promoted by exercise. Moreover, oral beta-adrenergic receptor blockade did not prevent exercise-induced lipid mobilization in SCAT while exerting fat cell beta-adrenergic receptor blockade. Exercise-induced increase in plasma ANP was potently amplified by oral tertatolol. A positive correlation was found between EGC and plasma ANP levels but also between extracellular cGMP (i.e., index of ANP-mediated lipolysis) and EGC. Thus, we demonstrate that exercise-induced lipid mobilization resistant to local propranolol and lipid-mobilizing action observed under oral beta-blockade is related to the action of ANP. Oral beta-adrenergic receptor blockade, which potentiates exercise-induced ANP release by the heart, may contribute to lipid mobilization in SCAT. The potential relevance of an ANP-related lipid-mobilizing pathway is discussed.
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        Exercise-induced lipid mobilization in subcutaneous adipose tissue is mainly related to natriuretic peptides in overweight men.

        Involvement of sympathetic nervous system and natriuretic peptides in the control of exercise-induced lipid mobilization was compared in overweight and lean men. Lipid mobilization was determined using local microdialysis during exercise. Subjects performed 35-min exercise bouts at 60% of their maximal oxygen consumption under placebo or after oral tertatolol [a beta-adrenergic receptor (AR) antagonist]. Under placebo, exercise increased dialysate glycerol concentration (DGC) in both groups. Phentolamine (alpha-AR antagonist) potentiated exercise-induced lipolysis in overweight but not in lean subjects; the alpha(2)-antilipolytic effect was only functional in overweight men. After tertatolol administration, the DGC increased similarly during exercise no matter which was used probe in both groups. Compared with the control probe under placebo, lipolysis was reduced in lean but not in overweight men treated with the beta-AR blocker. Tertatolol reduced plasma nonesterified fatty acids and insulin concentration in both groups at rest. Under placebo or tertatolol, the exercise-induced changes in plasma nonesterified fatty acids, glycerol, and insulin concentrations were similar in both groups. Exercise promoted a higher increase in catecholamine and ANP plasma levels after tertatolol administration. In conclusion, the major finding of our study is that in overweight men, in addition to an increased alpha(2)-antilipolytic effect, the lipid mobilization in subcutaneous adipose tissue that persists during exercise under beta-blockade is not dependent on catecholamine action. On the basis of correlation findings, it seems to be related to a concomitant exercise-induced rise in plasma ANP when exercise is performed under tertatolol intake and a decrease in plasma insulin.
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          Comparison of passive heat or exercise-induced dehydration on renal water and electrolyte excretion: the hormonal involvement.

          The effects of hydromineral hormones and catecholamines on renal water and electrolyte excretion were examined during and after dehydration induced by either passive heat or exercise. Eight healthy young Caucasian subjects participated in three separate trials, each including three consecutive phases. Phases 1 and 3 involved a 90-min period at rest in a thermoneutral environment, while phase 2 involved a 120-min period designed to provide: (1) euhydration (control trial), (2) passive heat-induced dehydration of 2.8% body mass, or (3) exercise-induced dehydration of 2.8% body mass. During the two dehydration procedures, the decreases in urine flow and sodium excretion were more marked during exercise (P < 0.05). An increase in plasma catecholamines occurred only during exercise, together with a reduction in creatinine clearance and more marked increases in plasma renin and aldosterone than during passive heat exposure (P < 0.05). Although plasma vasopressin was elevated during the two dehydration procedures, urine osmolality did not change and, moreover, free water clearance increased during exercise (P < 0.05). Plasma levels of atrial natriuretic peptide increased markedly only during exercise compared to the other trials (P < 0.05). After the dehydration procedures, urine flow decreased again and urine osmolality increased markedly (P < 0.05), while plasma vasopressin remained elevated. These results suggest that sympathoadrenal activation during exercise plays a major role in the more marked reduction in diuresis and natriuresis than during passive heat exposure. Despite high plasma vasopressin concentrations during the two dehydrating events, the observed antidiuresis was not due to an increased renal concentrating ability, and the vasopressin was more effective after the dehydration procedures.

            Author and article information

            [1 ]Departamento de Morfologia e Fisiologia, Faculdade de Medicina do ABC. Av. Príncipe de Gales, 821. 09060-650, Santo André, SP, Brazil
            [2 ]Escola de Artes, Ciência e Humanidades da Universidade de São Paulo (USP). Rua Arlindo Béttio, 1000, São Paulo, SP. 03828-000, Brazil
            [3 ]Departamento de Fisioterapia, Faculdade de Ciências e Tecnologia, Universidade Estadual Paulista, UNESP. Rua Roberto Simonsen, 305. 19060-900, Presidente Prudente, São Paulo, Brazil
            [4 ]Departamento de Saúde Coletiva, Universidade Federal do Acre. Campus Universitário, BR 364, Km 04. 69915-900, Rio Branco, AC, Brasil
            [5 ]Departamento de Fonoaudiologia, Faculdade de Filosofia e Ciências, Universidade Estadual Paulista, UNESP. Av. Higyno Muzzi Filho, 737. 17.525-900, Marília, SP, Brazil
            Int Arch Med
            Int Arch Med
            International Archives of Medicine
            BioMed Central
            7 February 2012
            : 5
            : 4
            Copyright ©2012 de Almeida et al; licensee BioMed Central Ltd.

            This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.




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