Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction

Clavell, Alfredo L.; Stingo, A. J.; Aarhus, Lawrence L.; Burnett, John C.

doi:10.1152/ajpregu.1993.265.6.r1416

Cited by 10 publications

(13 citation statements)

References 22 publications

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“…In the present study, the lack of effect of ANP and BNP on PRA levels presumably reflects a balance of inhibitory actions on the juxtaglomerular apparatus (through high circulatory levels of natriuretic peptides and enhanced delivery of sodium and chloride to the macula densa) and the stimulatory effect on the afferent arteriolar baroreceptor (through the fall in renal artery perfusion pressure). Indeed, these findings are in agreement with other studies where the failure of BNP to suppress PRA was associated with a significant hypotensive response [13]. Despite the absence of PRA change during the peptide infusions, plasma aldosterone was significantly reduced by both ANP and BNP, indicating a direct inhibitory effect of the peptides on the adrenal gland.…”

Section: I63supporting

confidence: 92%

“…The fall in preload is likely to be mediated by a decrease in circulating volume and venous return (indicated by the rise in haematocrit), possibly through redistribution of plasma volume to the extravascular space [5] and through urinary loss (as evidenced by the significant diuresis in the later 2 h of the infusions). Similar haemodynamic effects have been observed by others during administration of ANP [ l l , 121 and BNP [13,141 in experimental models and in human heart failure. CO was not altered compared with a control by either ANP or BNP in the present study.…”

Section: I63supporting

confidence: 86%

“…CO was not altered compared with a control by either ANP or BNP in the present study. Previous investigations looking at ANP infusion in heart failure have observed either no change in CO [lo] or a rise [ll], whilst BNP has been shown to increase CO in human heart failure [14] and induce a decrease in a model of thoracic vena caval constriction [13]. These variable responses presumably depend upon the relative changes in afterload and preload in the setting of cardiac failure.…”

Section: I63mentioning

confidence: 99%

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Comparative Bioactivity of Atrial and Brain Natriuretic Peptides in An Ovine Model of Heart Failure

et al. 1997

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1. Whereas many studies have detailed the effects of exogenous atrial natriuretic peptide (ANP) infusions in heart failure, and a limited number have examined the effects of brain natriuretic peptide (BNP), none have directly compared the bioactivity of similar doses of ANP and BNP under standard conditions of impaired cardiac function. We compared the hormonal, haemodynamic and renal effects of 3 h infusions of ANP, BNP and a vehicle control in eight sheep with pacing-induced heart failure (225 beats/min for 8-12 days). 2. Infusion of ANP and BNP increased plasma ANP (P < 0.001) (276 +/- 27 versus control 142 +/- 26 pmol/l) and BNP (P < 0.001) (257 +/- 34 versus control 45 +/- 5 pmol/l) respectively, in association with increased cyclic 3',5'-guanosine monophosphate [control, 40 +/- 6; ANP, 53 +/- 6 (P < 0.05); BNP, 57 +/- 7 nmol/l (P < 0.001)]. Metabolic clearance rate and half-life were similar for both peptides. Infusion of ANP and BNP similarly reduced mean arterial pressure [control, 73.0 +/- 1.6; ANP, 67.6 +/- 1.2 (P < 0.01); BNP, 65.7 +/- 1.7 mmHg (P < 0.001)], left atrial pressure (both P < 0.05) (control, 22.0 +/- 0.7; ANP, 19.9 +/- 1.0; BNP, 19.8 +/- 0.9 mmHg) and peripheral resistance [control, 50.3 +/- 4.1 mmHg l-1 min-1; ANP, 46.0 +/- 2.8 (P < 0.05); BNP, 43.8 +/- 4.5 (P < 0.01)], and increased urine volume (2-3-fold, both P < 0.05), sodium excretion (> 10-fold, both P < 0.01) and haematocrit levels relative to control (both P < 0.05). Infused BNP tended to raise plasma ANP levels (by 28 pmol/l), while ANP increased plasma BNP (by 18 pmol/l). Plasma aldosterone was reduced by approximately 40% by both peptides (both P < 0.05). 3. In conclusion, ANP and BNP are both powerfully, natriuretic, similarly suppress aldosterone and appear equipotent in reducing preload and afterload in this model of pacing-induced heart failure.

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Section: I63supporting

confidence: 92%

Section: I63supporting

confidence: 86%

Section: I63mentioning

confidence: 99%

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Comparative Bioactivity of Atrial and Brain Natriuretic Peptides in An Ovine Model of Heart Failure

et al. 1997

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“…36,37 Extensive previous studies have demonstrated the ability of human BNP to have potent cardiorenal and humoral actions in the dog. 38 Indeed, human BNP activates cGMP generation in isolated canine glomeruli. 39 While our results suggest comparable actions between M-ANP and human BNP our conclusions need to be cautious due to differences in human and canine BNP.…”

Section: Discussionmentioning

confidence: 99%

A Novel Atrial Natriuretic Peptide Based Therapeutic in Experimental Angiotensin II Mediated Acute Hypertension

et al. 2010

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M-atrial natriuretic peptide (M-ANP) is a novel next generation 40 amino acid peptide based on atrial natriuretic peptide (ANP), which is highly resistant to enzymatic degradation and has greater and more sustained beneficial actions compared to ANP. The current study was designed to advance our understanding of the therapeutic potential of M-ANP in a canine model of acute angiotensin II induced hypertension with elevated cardiac filling pressures and aldosterone activation. We compare M-ANP to vehicle and equimolar human B-type natriuretic peptide (BNP), which possesses the most potent in vivo actions of the native natriuretic peptides. M-ANP significantly lowered mean arterial pressure and systemic vascular resistance. Importantly, despite a reduction in blood pressure, renal function was enhanced with significant increases in renal blood flow, glomerular filtration rate, diuresis, and natriuresis following M-ANP infusion. While angiotensin II induced an acute increase in pulmonary capillary wedge pressure, M-ANP significantly lowered pulmonary capillary wedge pressure, pulmonary artery pressure, and right atrial pressure. Further, M-ANP significantly suppressed angiotensin II induced activation of aldosterone. These cardiovascular and renal enhancing actions of M-ANP were accompanied by significant increases in plasma and urinary cGMP, the second messenger molecule of the natriuretic peptide system. When compared to human BNP, M-ANP had comparable cardiovascular actions but resulted in a greater natriuretic effect. These results suggest that M-ANP, which is more potent than ANP in normal canines, has potent blood pressure lowering and renal enhancing properties and may therefore serve as an ANP based therapeutic for acute hypertension.

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“…Plasma and heart ANP, BNP, and CNP immunoreactivities were determined with a double-antibody radioimmunoassay as previously described. 11,25,26 Protein assay was conducted with a DC Protein assay kit (BioRad).…”

Section: Measurement Of Plasma and Heart Concentrations Of Natriuretimentioning

confidence: 99%

Vasopeptidase Inhibition Prevents Endothelial Dysfunction of Resistance Arteries in Salt-Sensitive Hypertension in Comparison With Single ACE Inhibition

d’Uscio

Quaschning

Burnett³

et al. 2001

Hypertension

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Abstract-To determine whether natriuretic peptides in addition to the renin-angiotensin system are involved in functional and structural vascular changes in salt-sensitive hypertension, we compared equipotent hypotensive treatment with the dual neutral endopeptidase/ACE inhibitor omapatrilat (35 mg ⅐ kg Ϫ1 ⅐ d Ϫ1) or the ACE inhibitor captopril (100 mg ⅐ kg). The reactivity and geometry of mesenteric resistance arteries from Dahl salt-sensitive rats were studied in vitro under perfused and pressurized conditions. Chronic salt administration increased systolic blood pressure by 57Ϯ4 mm Hg, whereas concentrations of atrial natriuretic peptide were reduced in heart and in plasma (PϽ0.05). In addition, the medial cross-sectional area of small mesenteric arteries was increased and endothelium-dependent relaxation in response to acetylcholine and contraction in response to endothelin-1 were impaired in the mesenteric arteries of salt-sensitive rats on a high-salt diet (PϽ0.05). Concomitant treatment with either omapatrilat or captopril reduced the increase in systolic blood pressure and hypertrophic remodeling to a similar degree (PϽ0.05) but affected plasma and cardiac atrial natriuretic peptide levels differently (PϽ0.05). In addition, omapatrilat normalized endothelium-dependent relaxations to a greater extent than captopril (PϽ0.05). Furthermore, vasopeptidase inhibition increased cGMP levels compared with captopril (PϽ0.05). Contractions to endothelin-1 were normalized by either antihypertensive drug. These results suggest that in the Dahl rat, with similar reductions in systolic blood pressure, omapatrilat is superior to captopril in preventing impaired endothelial function in small resistance arteries. Thus, vasopeptidase inhibition may have therapeutic advantages of the prevention of changes in vascular function and structure in salt-sensitive forms of hypertension. The vascular endothelium is a source of vasoactive substances such as NO, 3 as well as endothelin-1 (ET-1) 4 and angiotensin, 5,6 that modulate vascular smooth muscle cell (VSMC) tone and proliferation. NO is a potent vasodilator and is formed from L-arginine by endothelial NO synthase. 7 Vasodilation in response to abluminal release of endothelium-derived NO is associated with an increase in cGMP in VSMCs. 8 The natriuretic peptide family consists of 3 peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). 2 ANP is a potent natriuretic and vasoactive peptide that is produced predominantly in the atrial myocytes; BNP is mainly produced by the left ventricle of the heart. 9,10 Both peptides are released into the circulation and thus play an important role as autocrine mediators in the control of cardiorenal homeostasis and of vascular tone. 11 In contrast, CNP is of endothelial origin and plays a paracrine role in the regulation of vascular tone and structure. 12-14 Natriuretic peptides are degraded by neutral endopeptidase (NEP), which is widely distributed in endothelial cells, VSMCs, car...

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Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction

Cited by 10 publications

References 22 publications

Comparative Bioactivity of Atrial and Brain Natriuretic Peptides in An Ovine Model of Heart Failure

Comparative Bioactivity of Atrial and Brain Natriuretic Peptides in An Ovine Model of Heart Failure

A Novel Atrial Natriuretic Peptide Based Therapeutic in Experimental Angiotensin II Mediated Acute Hypertension

Vasopeptidase Inhibition Prevents Endothelial Dysfunction of Resistance Arteries in Salt-Sensitive Hypertension in Comparison With Single ACE Inhibition

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