***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: To determine the major stimuli for the release of brain natriuretic peptide ( BNP ) and atrial natriuretic peptide ( ANP ) , we measured their plasma concentrations in 14 normal subjects and 19 patients with essential hypertension during exercise with a bicycle ergometer .  The plasma levels of both hormones at baseline were significantly higher in the hypertensive group than in the controls ( p < 0.05 ) . The exercise raised both the plasma BNP and ANP , with concomitant increases in systolic blood pressure ( SBP ) , heart rate ( HR ) and plasma norepinephrine ( NE ) or epinephrine ( Epi ) in each group . In the controls the change in ANP correlated with those in SBP , HR and NE ( p < 0.05 ) , and similarly the change in BNP with those in SBP , HR , NE and Epi ( p < 0.05 ) . In multivariate regression analysis only NE was found to be a significant stimulus for ANP secretion , whereas SBP or Epi was related to BNP release . In the hypertensives the change in ANP correlated with those in HR and NE , but on multivariate regression analysis the change in ANP correlated only with that in HR . The change in BNP in the hypertensives correlated only with that in HR . These findings indicate that in normal subjects the exercise-induced release of BNP and ANP is more sensitive to a similar but slightly different sympathetic stimulus , whereas in hypertensives the major stimulus for the release of both hormones is heart rate , indicating that the mediators for BNP or ANP release are altered by some factors involved in hypertension OBJECTIVE Heart failure is common in individuals with type 2 diabetes , and early detection of individuals at risk may offer opportunities for prevention . We aim ed to explore 1 ) prospect i ve associations of  B-type natriuretic peptide ( BNP )  levels in a non – heart failure range with changes in markers of left ventricular ( LV ) function and 2 ) possible effect modification by type 2 diabetes in a population -based cohort . RESEARCH DESIGN AND METHODS Echocardiographic measurements were performed at baseline ( 2000–2001 ) and follow-up ( 2007–2009 ) , together with st and ardized physical examinations and BNP measurements on 300 individuals ( mean age 66 years , 32 % with type 2 diabetes ) of the longitudinal Hoorn Study . Multivariate linear regression analyses were performed to investigate associations of baseline BNP ( < 100 pg/mL ) in individuals without prevalent heart failure at baseline with changes in LV mass index , LV ejection fraction , left atrial volume index , and ratio of early diastolic LV inflow velocity ( E ) to early diastolic lengthening velocity ( e′ ) ( E/e′ ) . RESULTS In all individuals , higher BNP was associated with 8-year increases in left atrial volume index . Higher BNP was also associated with increasing LV mass index and E/e′. These associations were significantly stronger in individuals with type 2 diabetes compared with the nonsignificant associations in individuals without type 2 diabetes . CONCLUSIONS This 8-year follow-up study shows that higher BNP levels in a non – heart failure range were associated with an increased LV mass and deteriorated LV diastolic function , particularly in individuals with type 2 diabetes . This implies that the presence or absence of type 2 diabetes should be taken into account if BNP levels are used to assess future heart failure risk OBJECTIVE —Atrial natriuretic peptide ( ANP ) regulates arterial blood pressure . In addition , ANP has recently been shown to promote human adipose tissue lipolysis through cGMP-mediated hormone-sensitive lipase activation . We hypothesized that ANP increases postpr and ial free fatty acid ( FFA ) availability and energy expenditure while decreasing arterial blood pressure . RESEARCH DESIGN AND METHODS —We infused human ANP ( 25 ng · kg−1 · min−1 ) in 12 men ( age 32 ± 0.8 years , BMI 23.3 ± 0.4 kg/m2 ) before , during , and 2 h after ingestion of a st and ardized high-fat test meal in a r and omized , double-blind , cross-over fashion . Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings . Metabolism was monitored through venous blood sampling , intramuscular and subcutaneous abdominal adipose tissue microdialysis , and indirect calorimetry . RESULTS —ANP infusion decreased mean arterial blood pressure by 4 mmHg during the postpr and ial phase ( P < 0.01 vs. placebo ) . At the same time , ANP induced lipolysis systemically ( P < 0.05 vs. placebo ) and locally in subcutaneous abdominal adipose tissue ( P < 0.0001 vs. placebo ) , leading to a 50 % increase in venous glycerol ( P < 0.01 ) and FFA ( P < 0.05 ) concentrations compared with placebo . The increase in FFA availability with ANP was paralleled by a 15 % increase in lipid oxidation rates ( P < 0.05 vs. placebo ) , driving a substantial increase in postpr and ial energy expenditure ( P < 0.05 vs. placebo ) . CONCLUSIONS —Our data identify the ANP system as a novel pathway regulating postpr and ial lipid oxidation , energy expenditure , and concomitantly arterial blood pressure . The findings could have therapeutic implication BACKGROUND The natriuretic peptides are counterregulatory hormones involved in volume homeostasis and cardiovascular remodeling . The prognostic significance of plasma natriuretic peptide levels in apparently asymptomatic persons has not been established . METHODS We prospect ively studied 3346 persons without heart failure . Using proportional-hazards regression , we examined the relations of plasma B-type natriuretic peptide and N-terminal pro-atrial natriuretic peptide to the risk of death from any cause , a first major cardiovascular event , heart failure , atrial fibrillation , stroke or transient ischemic attack , and coronary heart disease . RESULTS During a mean follow-up of 5.2 years , 119 participants died and 79 had a first cardiovascular event . After adjustment for cardiovascular risk factors , each increment of 1 SD in log B-type natriuretic peptide levels was associated with a 27 percent increase in the risk of death ( P=0.009 ) , a 28 percent increase in the risk of a first cardiovascular event ( P=0.03 ) , a 77 percent increase in the risk of heart failure ( P<0.001 ) , a 66 percent increase in the risk of atrial fibrillation ( P<0.001 ) , and a 53 percent increase in the risk of stroke or transient ischemic attack ( P=0.002 ) . Peptide levels were not significantly associated with the risk of coronary heart disease events . B-type natriuretic peptide values above the 80th percentile ( 20.0 pg per milliliter for men and 23.3 pg per milliliter for women ) were associated with multivariable-adjusted hazard ratios of 1.62 for death ( P=0.02 ) , 1.76 for a first major cardiovascular event ( P=0.03 ) , 1.91 for atrial fibrillation ( P=0.02 ) , 1.99 for stroke or transient ischemic attack ( P=0.02 ) , and 3.07 for heart failure ( P=0.002 ) . Similar results were obtained for N-terminal pro-atrial natriuretic peptide . CONCLUSIONS In this community-based sample , plasma natriuretic peptide levels predicted the risk of death and cardiovascular events after adjustment for traditional risk factors . Excess risk was apparent at natriuretic peptide levels well below current thresholds used to diagnose heart failure BACKGROUND Now that marathon racing is growing in popularity , many thous and s of enthusiastic athletes are participating in various ultramarathons all over the world each year . However , it remains controversial whether such a sport contributes to the promotion of health . The occurrence of transient cardiac dysfunction and irreversible myocardial injury has been reported in association with such exercise in healthy individuals . Brain natriuretic peptide ( BNP ) is a cardiac hormone , as is atrial natriuretic peptide ( ANP ) , and its measurement has been widely used for clinical evaluation of cardiac dysfunction . However , little is known about the response of plasma BNP to prolonged strenuous exercise . We hypothesized that confirmation of minimal cardiac dysfunction or myocardial injury may be made by measurements of plasma BNP . METHODS Levels of plasma ANP , BNP , catecholamines , blood lactate , and serum cardiac troponin T ( cTnT )  were determined before and after a 100-km ultramarathon in 10 healthy men to examine the effects of the exercise on levels of ANP and BNP and correlations between the natriuretic peptides and cTnT as a marker for myocardial damage . RESULTS Whereas all variables significantly increased after the race , increased levels of ANP and BNP were most strongly correlated with increases in cTnT levels . The cTnT level after the race was greater than the upper reference limit in 9 of 10 men . CONCLUSIONS Such exercise significantly increased ANP and BNP levels  in healthy men , and the increases could be partially attributed to myocardial damage during the race BACKGROUND C-type natriuretic peptide ( CNP ) is structurally related to cardiac natriuretic peptides and is currently considered as an endothelium-derived hyperpolarizing factor . Endothelial dysfunction , commonly observed in chronic heart failure ( HF ) patients is positively affected by physical training . METHODS To evaluate the effect of aerobic physical training on the expression of CNP , 90 HF patients on optimal pharmacological treatment ( age 62+/-2 years , mean+/-SEM ) , r and omly assigned in a 3 : 1 ratio to either control group ( C , 19 patients ) or home-based aerobic exercise-training program group ( T , 71 patients ) , completed the protocol . Plasma assay of CNP , brain natriuretic peptide or B-type natriuretic peptide ( BNP ) , and norepinephrine ; echocardiogram ; and cardiopulmonary-stress test  were performed in all patients at enrollment and after 9 months . RESULTS At baseline , in both groups , CNP plasma level was significantly related to BNP ( R=0.50 ) , ejection fraction ( R=0.43 ) , and peak oxygen uptake ( VO2 , R=0.43 , all P<0.001 ) . After 9 months , trained patients showed an improvement in peak VO2 ( P<0.001 ) and ejection fraction ( P<0.05 ) , whereas norepinephrine ( P<0.05 ) , BNP ( P<0.001 ) , and CNP ( P<0.001 ) decreased . No changes occurred in group C. In group T , the decrease in CNP was significantly related to the increase in peak VO2 ( R=0.31 , P<0.01 ) , and the relation between CNP and BNP was preserved at the end of the program ( R=0.41 , P<0.001 ) . CONCLUSION Clinical and functional improvement after physical training in HF patients is associated with a decrease in adrenergic activation and in both CNP and BNP concentration . Changes in CNP plasma concentration after physical training might reflect an improvement in endothelial function BACKGROUND Walking is associated with reduced diabetes incidence , but few studies have examined whether it reduces mortality among those who already have diabetes . OBJECTIVE To estimate the association between walking and the risk for all-cause and cardiovascular disease ( CVD ) mortality among persons with diabetes . DESIGN Prospect i ve cohort study of a representative sample of the US population . SETTING Interviewer-administered survey in the general community . PARTICIPANTS We sample d 2896 adults 18 years and older with diabetes as part of the 1990 and 1991 National Health Interview Survey . MAIN OUTCOME MEASURE All-cause and CVD mortality for 8 years . RESULTS Compared with inactive individuals , those who walked at least 2 h/wk had a 39 % lower all-cause mortality rate ( hazard rate ratio [ HRR ] , 0.61 ; 95 % confidence interval [ CI ] , 0.48 - 0.78 ; 2.8 % vs 4.4 % per year ) and a 34 % lower CVD mortality rate ( HRR , 0.66 ; 95 % CI , 0.45 - 0.96 ; 1.4 % vs 2.1 % per year ) . We controlled for sex , age , race , body mass index ( calculated as weight in kilograms divided by the square of height in meters ) , smoking , and comorbid conditions . The mortality rates were lowest for persons who walked 3 to 4 h/wk ( all-cause mortality HRR , 0.46 ; 95 % CI , 0.29 - 0.71 ; CVD mortality HRR , 0.47 ; 95 % CI , 0.24 - 0.91 ) and for those who reported that their walking involved moderate increases in heart and breathing rates ( 
    Output:
    
In athletes and young , healthy subjects , the NP concentration at rest is not elevated , but strenuous endurance exercise significantly increases NPs .
The exercise-induced increase in NPs may be caused by transient myocardial wall stress , cardiomyocyte metabolic changes , or neuroendocrinological response , which may have cytoprotective and growth-regulating effects on the heart .
On the other h and , in elderly , overweight/obese subjects , and patients with hypertension , NP concentrations also increase during exercise ; however , NP secretion may be more susceptible to cardiac stress compared to young , healthy individuals .
Recent studies have shown that NPs are associated with thermogenesis in fat tissue and oxidative capacity in skeletal muscles .