Brain natriuretic peptide (BNP), originally identified in porcine brain tissue, is primarily secreted by the ventricular myocardium in response to increased ventricular blood volume and stretching . While initially named "brain natriuretic peptide," it is now often referred to as "B-type natriuretic peptide" to better reflect its source .
Oreochromis mossambicus, also known as tilapia, is a fish species used in studies of natriuretic peptides . Recombinant Oreochromis mossambicus brain natriuretic peptide (nppb) refers to a synthetically produced version of the BNP found in Oreochromis mossambicus . This recombinant protein is produced using genetic engineering techniques, allowing researchers to study its physiological effects and potential applications .
The physiological effects of BNP include:
Renal Effects: BNP dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells, increasing pressure in the glomerular capillaries and the glomerular filtration rate (GFR) . It also increases blood flow through the vasa recta, washing solutes out of the medullary interstitium, leading to less reabsorption of tubular fluid and increased excretion . Additionally, BNP decreases sodium reabsorption in the distal convoluted tubule and cortical collecting duct of the nephron and inhibits renin secretion, thereby inhibiting the renin–angiotensin–aldosterone system .
Adrenal Effects: BNP reduces aldosterone secretion by the zona glomerulosa of the adrenal cortex .
Vascular Effects: BNP relaxes vascular smooth muscle in arterioles and venules through membrane receptor-mediated elevation of vascular smooth muscle cGMP and inhibition of the effects of catecholamines . It also promotes uterine spiral artery remodeling, which is important for preventing pregnancy-induced hypertension .
Cardiac Effects: BNP inhibits maladaptive cardiac hypertrophy .
Adipose Tissue Effects: BNP increases the release of free fatty acids from adipose tissue, activating adipocyte plasma membrane type A guanylyl cyclase receptors NPR-A and increasing intracellular cGMP levels that induce the phosphorylation of a hormone-sensitive lipase and perilipin A via the activation of a cGMP-dependent protein kinase-I (cGK-I) .
Recombinant human brain natriuretic peptide (rh-BNP) is a synthetic analog of BNP that binds to type A natriuretic peptide receptors and activates guanylyl cyclase (GC), leading to an intracellular rise in cGMP . This process activates cGMP-dependent protein kinase (PKG), producing vascular smooth muscle relaxation effects on both arteries and veins .
Clinical applications and effects of recombinant human BNP:
Acute Decompensated Heart Failure: rhBNP has positive cardiac effects in patients with acute decompensated heart failure . It reduces peripheral circulation resistance and the resistance to venous return .
Improved Cardiac Output: rhBNP significantly increases cardiac output by reducing peripheral circulation resistance and the resistance to venous return .
Vasodilation: rhBNP exerts vasodilatory effects by decreasing systemic vascular resistance (SVR) and resistance to venous return (RVR) .
Diuretic Effect: rhBNP has a diuretic effect, which helps to reduce blood volume .
Improved Quality of Life: rhBNP therapy can improve heart function and reduce microinflammation in patients with chronic heart failure, leading to a better quality of life .
A study involving 102 chronic heart failure (HF) patients examined the safety and efficacy of lyophilized recombinant BNP . The patients were randomly assigned to either a control group or an observation group . The recombinant human BNP group showed better physical, emotional, social, and economic scores, as well as improved cardiac function . The left ventricular ejection fraction and stroke volume were significantly higher in the observation group compared to the control group . Adverse reactions were similar between the two groups .
Recombinant human BNP affects various hemodynamic parameters. A study on patients undergoing rhBNP treatment showed the following changes:
| Hemodynamic Parameter | Baseline (T0) | 30 Minutes After rhBNP Infusion | 3 Hours After rhBNP Infusion |
|---|---|---|---|
| Cardiac Output (CO) (L/min) | 3.75 ± 1.14 | 4.24 ± 0.97 | 4.20 ± 1.19 |
| Mean Arterial Pressure (MAP) | N/A | Decreasing Trend | Decreasing Trend |
| Central Venous Pressure (CVP) | N/A | No Change | Significantly Increased |
| Heart Rate (HR) | N/A | Decreasing Trend | Decreasing Trend |
| Stroke Volume (SV) | N/A | Increasing Trend | Increasing Trend |
| Systemic Vascular Resistance (SVR) | 18.85 ± 7.66 | 14.62 ± 6.13 | No Change |
| Mean Systemic Filling Pressure (PMSF) | 32.71 ± 20.00 | Decreasing Trend | 28.254 ± 6.09 |
| Resistance to Venous Return (RVR) | 5.93 ± 4.97 | N/A | 4.46 ± 1.53 |
Recombinant Oreochromis mossambicus Brain natriuretic peptide (nppb) is a cardiac hormone with potential paracrine antifibrotic activity in the heart. It plays a crucial role in cardiovascular homeostasis through its effects on natriuresis, diuresis, vasorelaxation, and the inhibition of renin and aldosterone secretion.