Localization of Atrial Natriuretic Factor Receptors in the Mesenteric Arterial Bed

León, Héctor De; Bonhomme, Marie-Chantal; Thibault, Gaétan; García, Raúl

doi:10.1161/01.res.77.1.64

Cited by 31 publications

(7 citation statements)

References 39 publications

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“…Other authors have shown the presence of abundant clearance receptor binding and protein in adipocytes. 18,19,22 Moreover, plasma levels of ANP in obese hypertensives were found to be lower than those measured in obese normotensive individuals, together with higher gene expression of the clearance receptor for NP in adipose tissue. 24 These findings are consistent with the hypothesis that the increased total adipose mass of obese hypertensives, through the enhanced expression of the biologically inactive NPr-C, 14,15 might influence the activity of NP.…”

Section: Discussionmentioning

confidence: 93%

“…20,21 Other authors have shown the presence of abundant clearance receptor binding and protein in adipocytes. 22 Moreover, in adipose tissue NPr-C expression is dramatically inhibited by fasting, indicating a nutritional regulation of this receptor. 23 Plasma levels of ANP lower than that found in obese normotensive individuals have been shown in obese hypertensives, together with higher gene expression of the clearance receptor for NP in the adipose tissue.…”

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confidence: 99%

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Low Calorie Diet Enhances Renal, Hemodynamic, and Humoral Effects of Exogenous Atrial Natriuretic Peptide in Obese Hypertensives

et al. 1999

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The expression of the natriuretic peptide clearance receptor is abundant in human and rat adipose tissue, where it is specifically inhibited by fasting. In obese hypertensives, plasma atrial natriuretic peptide (ANP) levels were found to be lower than in obese normotensives. Therefore, the increased adipose mass might influence ANP levels and/or its biological activity. The aim of the present study was to evaluate whether the humoral, hemodynamic, and renal effects of exogenous ANP in obese hypertensives might be enhanced by a very low calorie diet. Eight obese hypertensives received a bolus injection of ANP (0.6 mg/kg) after 2 weeks of a normal calorie/normal sodium diet, and blood pressure (BP), heart rate, ANP, cGMP, plasma renin activity, and aldosterone were evaluated for 2 hours before and after the injection. Diuresis and natriuresis were measured every 30 minutes. The patients then started a low calorie/normal sodium diet (510 kcal/150 mmol/d) for 4 days, and then the ANP injection protocol was repeated. The low calorie diet induced a slight weight loss (from 90.61.1 to 87.71.2 kg; P0.01), which was accompanied by increase of cGMP excretion (from 146.010.1 to 154.59.5 nmol/24 h; P0.05) together with a reduction of BP (P0.01 versus basal levels). ANP injection after diet was followed by an increase of ANP levels similar to that observed before diet, but plasma cGMP, diuresis, and natriuresis increased significantly only after diet. Similarly, the decrease of BP after ANP administration was significantly higher after diet (change in mean arterial pressure, 6.40.7 versus 4.00.6 mm Hg; P0.05) as well as that of aldosterone (P0.01). These data show that a low calorie diet enhances the humoral, renal, and hemodynamic effects of ANP in obese hypertensives and confirm the importance of caloric intake in modulating the biological activity of ANP, suggesting that the natriuretic peptide system can play a role in the acute changes of natriuresis and diuresis associated with caloric restriction. (Hypertension. 1999;33:658-662.) Key Words: obesity hypertension natriuretic peptides, atrial cyclic GMP diuresis natriuresis S everal epidemiological and clinical studies have shown that excess weight and weight gain contribute to increase blood pressure (BP) in a large proportion of hypertensive patients. 1-3 Such studies have also demonstrated that BP in the adult is highly correlated to body mass index (BMI). 4,5 Although the association between obesity and hypertension is widely recognized, the pathophysiology of weight-related change in BP is a matter of debate. Several mechanisms have been suggested to play a role in the pathogenesis of obesity-related hypertension, such as increased plasma volume and cardiac output, 6 enhanced sympathetic nervous system activity , 7 hyperinsulinemia and insulin resistance, 8 and nutritional factors such as high sodium intake and/or sodium retention. 9 Moreover, the importance of weight gain per se in causing hypertension is reinforced by experimental studies showing that weight gain ...

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Section: Discussionmentioning

confidence: 93%

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confidence: 99%

Low Calorie Diet Enhances Renal, Hemodynamic, and Humoral Effects of Exogenous Atrial Natriuretic Peptide in Obese Hypertensives

et al. 1999

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“…NPR-A have also been identified in rat fat cells. 78,79 A weak ANP-stimulated increment of cGMP was reported in rat fat cells. 80 Human adipose tissue expresses NPR-A and NPR-C messenger RNA.…”

Section: Natriuretic Peptide Receptorsmentioning

confidence: 98%

An Unsuspected Metabolic Role for Atrial Natriuretic Peptides

Lafontan

Moro

Sengenès

et al. 2005

ATVB

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Abstract-In normal and obese humans, lipid mobilization and systemic nonesterified fatty acid levels are thought to be acutely controlled by catecholamines (ie, epinephrine and norepinephrine) and insulin. Natriuretic peptides (NPs) are known to play a key role in the regulation of salt and water balance and blood pressure homeostasis. They are involved in the pathophysiology of hypertension and heart failure. (ATP III). The NCEP definition of the metabolic syndrome includes 3 or more of the following: abdominal obesity, defined as waist circumference Ն102 cm in men and Ͼ88 cm in women; elevated triglyceride concentration Ն150 mg/dL, low HDL cholesterol (Ͻ40 mg/dL in men and Ͻ50 mg/dL in women); elevated fasting plasma glucose level (Ն110 mg/dL); and elevated blood pressure (Ն130/85 mm Hg). 1 The presence of abdominal obesity is more closely associated with the metabolic risk factors than body mass index. The prevalence of the metabolic syndrome increases with age. Obesity interferes with many metabolic pathways which underlie numerous potential risk factors. It is very difficult to differentiate between the major and minor factors, and some remain to be discovered. 2 This complexity leaves the area open and challenges basic and clinical researchers to uncover novel metabolic pathways. The discovery that cardiac natriuretic peptides (NPs) control human fat cell function is a provocative observation which reveals an unsuspected link between heart and adipose tissue. NPs exert potent lipolytic effects (eg, stimulation of hydrolysis of triacylglycerols stored in adipocytes) in isolated human fat cells. 3 When administered intravenously, they potently increase plasma glycerol and nonesterified fatty acid (NEFA) levels; in other words they stimulate lipid mobilization. 4 Before the discovery of the NP pathway, catecholamines and insulin were considered to be the major acute regulators of lipid mobilization in humans: they both act through a cAMP-dependent regulation of lipolysis. In contrast, NPs activate a 3Ј, 5Ј-cyclic guanosine monophosphate (cGMP)-dependent pathway that is completely independent from the cAMP-dependent pathway. 5 The NPs may represent a promising new pathway contributing to the control of lipid mobilization in humans in physiological and pathological conditions. The introductory section

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“…The affinity of all three peptides for the clearance receptor is similar (Koller et al, 1991;Suga et al, 1992). The distribution of the NP receptors varies among tissues (De Leon et al, 1995;Dos Reis et al, 1995). It appears to be transcriptionally regulated at different development stages (Brown and Chen, 1995) and in different physiological or pathological states (Yoshimoto et al, 1996), thus dictating the effects of the different NPs on a specific tissue.…”

Section: Guanylate Cyclasesmentioning

confidence: 99%

Molecular mechanism of cGMP-mediated smooth muscle relaxation

et al. 2000

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Contraction and relaxation of smooth muscle is a tightly regulated process involving numerous endogenous substances and their intracellular second messengers. We examine the key role of cyclic guanosine monophosphate (cGMP) in mediating smooth muscle relaxation. We briefly review the current art regarding cGMP generation and degradation, while focusing on the recent identification of the molecular mechanisms underlying cGMP-mediated smooth muscle relaxation. cGMP-induced SM relaxation is mediated mainly by cGMP-dependent protein kinase activation. It involves several molecular events culminating in a reduction in intracellular Ca(2+) concentration and a decrease in the sensitivity of the contractile system to Ca(2+). We propose that the cGMP-induced decrease in Ca(2+) sensitivity is a strategic way to achieve "active relaxation" of the smooth muscle. In summary, we present compelling evidence supporting a key role for cGMP as a mediator of smooth muscle relaxation in physiological and pharmacological settings.

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Localization of Atrial Natriuretic Factor Receptors in the Mesenteric Arterial Bed

Cited by 31 publications

References 39 publications

Low Calorie Diet Enhances Renal, Hemodynamic, and Humoral Effects of Exogenous Atrial Natriuretic Peptide in Obese Hypertensives

Low Calorie Diet Enhances Renal, Hemodynamic, and Humoral Effects of Exogenous Atrial Natriuretic Peptide in Obese Hypertensives

An Unsuspected Metabolic Role for Atrial Natriuretic Peptides

Molecular mechanism of cGMP-mediated smooth muscle relaxation

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