Natriuretic peptides comprise a family of 3 structurally related molecules: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). ANP and BNP act mainly as cardiac hormones, produced primarily by the atrium and ventricle, respectively. C-type natriuretic peptide occurs in a wide variety of tissues, where it acts as a local regulator. Natriuretic peptides can influence body fluid homeostasis and blood pressure control through the activation of 2 guanylyl cyclase-coupled natriuretic peptide receptor subtypes--GC-A and GC-B. The ANP and BNP genes are tightly linked on human chromosome 1 and mouse chromosome 4 (Steinhelper, 1993; Yang-Feng et al., 1985).
NCBI Summary:
This gene is a member of the natriuretic peptide family and encodes a secreted protein which functions as a cardiac hormone. The protein undergoes two cleavage events, one within the cell and a second after secretion into the blood. The protein's biological actions include natriuresis, diuresis, vasorelaxation, inhibition of renin and aldosterone secretion, and a key role in cardiovascular homeostasis. A high concentration of this protein in the bloodstream is indicative of heart failure. The protein also acts as an antimicrobial peptide with antibacterial and antifungal activity. Mutations in this gene have been associated with postmenopausal osteoporosis. [provided by RefSeq, Nov 2014]
General function
Ligand, Hormone
Comment
As reviewed by Valli et al. (1999), BNP is the second compound of a family of polypeptide hormones named natriuretic peptides. This peptide has great pathophysiologic importance as a stress-induced cardiac hormone secreted from ventricles, and it rises in several cardiac diseases. It promotes natriuresis and diuresis, acts as a vasodilator, and antagonizes the vasoconstrictor effects of the renin-angiotensin-aldosterone system.
Cellular localization
Secreted
Comment
Diagnostic potential of serum N-terminal pro-B-type brain natriuretic peptide level in detection of cardiac wall stress in women with polycystic ovary syndrome: a cross-sectional comparison study. Celik O et al. (2007) In addition to the negative effect on fertility, polycystic ovary syndrome (PCOS) has been associated with cardiac pathology. Brain natriuretic peptide (BNP) is a possible marker for cardiac risk, therefore we investigated whether N-terminal pro-B-type BNP (NT-proBNP) increases in women with PCOS compared with healthy women of comparable age and body mass index. Thirty women with PCOS and 30 healthy women not suffering from overt cardiac disease were involved in the study. Fasting insulin and serum NT-proBNP levels were measured, and M-Mode echocardiography was performed. Insulin resistance was calculated using the homeostasis model assessment insulin resistance index (HOMA-IR). PCOS subjects had higher NT-proBNP levels than the control subjects (P < 0.001). Abnormal echocardiography indices were detected in 14 of the PCOS subjects (but none of the controls), including valvular heart disease in nine, diastolic dysfunction in two, right ventricular enlargement in one, right atrial enlargement in one and pulmonary hypertension in one. PCOS subjects (n = 30) showed an increased left ventricular mass (LVM) (P < 0.001) and left ventricular posterior wall thickness (LVPWT) (P = 0.006). In addition, NT-proBNP concentration was positively correlated with LVM (r = 0.587, P = 0.001) and negatively correlated with sex-hormone-binding globulin (r = -0.528, P = 0.003). There was a positive correlation between LVM and HOMA-IR (r = 0.295, P = 0.03) while LVPWT was positively correlated with fasting insulin and HOMA-IR (r = 0.335, P = 0.031 and r = 0.346, P = 0.045, respectively) in PCOS subjects (n = 30). The present study demonstrated that the level of NT-proBNP was increased in PCOS subjects with asymptomatic heart disease.//////////////////
Ovarian function
Oocyte maturation
Comment
Brain natriuretic peptide and C-type natriuretic peptide maintain porcine oocyte meiotic arrest. Zhang W 2014 et al.
Recent studies have shown that C-type natriuretic peptide (CNP) serves as a key control system during mouse oocyte maturation. We used pig models (in vitro and in vivo) to explore the role played by the natriuretic peptide family in porcine oocyte maturation. We reported the expression and location of natriuretic peptide system in different stages of porcine antral follicles. Atrial natriuretic peptide (ANP) and CNP were expressed primarily in granulosa cells, whereas brain natriuretic peptide (BNP) and natriuretic peptide receptor-B (NPRB) receptor were expressed in granulosa cells (both cumulus and mural granulosa cells) and thecal internal cells, and the natriuretic peptide receptor-A (NPRA) receptor predominantly in thecal cells. Upon in vitro culture, BNP and CNP maintained meiotic arrest of oocytes associated with cumulus cells. The expression levels of BNP, CNP, and the NPRB receptor increased upon treatment of prepubertal gilts with pregnant mare's serum gonadotropin and decreased upon subsequent human chorionic gonadotropin injection. Such dynamic changes in the expression of natriuretic peptides and their receptor paralleled the proportions of oocytes exhibiting nuclear maturation in vivo. These data indicated that BNP and CNP co-contributed to maintaining porcine meiotic arrest under physiological condition and lutenizing hormone (LH) relieved this inhibitory effect by decreasing the expression levels of BNP and CNP in vivo. Our present work, combined with previous data, improved the understanding of the oocyte meiotic arrest mechanisms and further revealed that natriuretic peptides serve as oocyte maturation inhibitor (OMI) to inhibit oocyte maturation in mammals. ? 2014 Wiley Periodicals, Inc.
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Since C-type natriuretic peptide (CNP), and the guanylyl cyclase receptors A and B (GC-A and GC-B) showed coordinate estrous cycle-dependent variation with maximal expression at proestrus, it was concluded that the natriuretic peptides (including BNP) may play an important role in either the development of ovulatory follicles or in the ovulatory process (Jankowski et al., 1997).
Expression regulated by
Comment
Ovarian localization
Cumulus, Granulosa
Comment
Follicle stages
Comment
Phenotypes
PCO (polycystic ovarian syndrome)
Mutations
1 mutations
Species: mouse
Mutation name: BNP
type: targeted overexpression fertility: unknown Comment:Suda et al. (1998) reported marked skeletal overgrowth in transgenic mice that overexpress BNP. Transgenic mice with elevated plasma BNP concentrations exhibited deformed bony skeletons characterized by kyphosis, elongated limbs and paws, and crooked tails. Studies using an in vitro organ culture of embryonic mouse tibias showed that BNP increases the height of cartilaginous primordium directly, thereby stimulating the total longitudinal bone growth. No skeletal defects had been reported in transgenic mice overexpressing ANP. Plasma BNP concentrations were markedly elevated in patients with congestive heart failure. Skeletal overgrowth may be exaggerated in BNP-transgenic mice because growth plates remain open for a long time in rodents. An association has been described between congenital heart diseases and scoliosis (Jordan et al., 1972; Reckles et al., 1975). Suda et al. (1998) speculated that overproduction of BNP and/or ANP by the heart might increase bone growth in patients with congenital heart defects, while growth plates are open.