Hormone that plays a key role in mediating cardio-renal homeostasis, and is involved in vascular remodeling and regulating energy metabolism (By similarity). Acts by specifically binding and stimulating NPR1 to produce cGMP, which in turn activates effector proteins, such as PRKG1, that drive various biological responses (By similarity). Regulates vasodilation, natriuresis, diuresis and aldosterone synthesis and is therefore essential for regulating blood pressure, controlling the extracellular fluid volume and maintaining the fluid-electrolyte balance (By similarity). Also involved in inhibiting cardiac remodeling and cardiac hypertrophy by inducing cardiomyocyte apoptosis and attenuating the growth of cardiomyocytes and fibroblasts (By similarity). Plays a role in female pregnancy by promoting trophoblast invasion and spiral artery remodeling in uterus, and thus prevents pregnancy-induced hypertension (By similarity). In adipose tissue, acts in various cGMP- and PKG-dependent pathways to regulate lipid metabolism and energy homeostasis (By similarity). This includes up-regulating lipid metabolism and mitochondrial oxygen utilization by activating the AMP-activated protein kinase (AMPK), and increasing energy expenditure by acting via MAPK11 to promote the UCP1-dependent thermogenesis of brown adipose tissue (By similarity). Binds the clearance receptor NPR3 which removes the hormone from circulation (By similarity). May have a role in cardio-renal homeostasis through regulation of natriuresis, diuresis, vasodilation, and inhibiting aldosterone synthesis. In vitro, promotes the production of cGMP and induces vasodilation. May promote natriuresis, at least in part, by enhancing prostaglandin E2 synthesis resulting in the inhibition of renal Na+-K+-ATPase (By similarity). However reports on the involvement of this peptide in mammal blood volume and blood pressure homeostasis are conflicting; according to a report, in vivo it is not sufficient to activate cGMP and does not inhibit collecting duct transport nor effect diuresis and natriuresis (By similarity). Appears to bind to specific receptors that are distinct from the receptors bound by atrial natriuretic peptide and vessel dilator. Possibly enhances protein excretion in urine by decreasing proximal tubular protein reabsorption (By similarity). May have a role in cardio-renal homeostasis through regulation of natriuresis, diuresis, and vasodilation. In vitro, promotes the production of cGMP and induces vasodilation. May promote natriuresis, at least in part, by enhancing prostaglandin E2 synthesis resulting in the inhibition of renal Na+-K+-ATPase. However reports on the involvement of this peptide in mammal blood volume and blood pressure homeostasis are conflicting; according to a report it is not sufficient to activate cGMP and does not inhibit collecting duct transport nor effect diuresis and natriuresis. Appears to bind to specific receptors that are distinct from the receptors bound by the atrial natriuretic and long-acting natriuretic peptides. Possibly functions in protein excretion in urine by maintaining the integrity of the proximal tubules and enhancing protein excretion by decreasing proximal tubular protein reabsorption. May have a role in cardio-renal homeostasis through regulation of diuresis and inhibiting aldosterone synthesis. In vitro, promotes the production of cGMP and induces vasodilation. May promote natriuresis, at least in part, by enhancing prostaglandin E2 synthesis resulting in the inhibition of renal Na+-K+-ATPase. May have a role in potassium excretion but not sodium excretion (natriuresis). Possibly enhances protein excretion in urine by decreasing proximal tubular protein reabsorption. Hormone produced in the kidneys that appears to be important for maintaining cardio-renal homeostasis. Mediates vasodilation, natriuresis and diuresis primarily in the renal system, in order to maintain the extracellular fluid volume and control the fluid-electrolyte balance. Specifically binds and stimulates cGMP production by renal transmembrane receptors, likely NPR1. Urodilatin not ANP, may be the natriuretic peptide responsible for the regulation of sodium and water homeostasis in the kidney. May have a role in cardio-renal homeostasis through regulation of natriuresis and vasodilation. In vivo promotes natriuresis and in vitro, vasodilates renal artery strips. May have a role in cardio-renal homeostasis through regulation of natriuresis and vasodilation. In vivo promotes natriuresis and in vitro, vasodilates renal artery strips. May have a role in cardio-renal homeostasis through regulation of regulation of natriuresis and vasodilation. In vivo promotes natriuresis. In vitro, vasodilates intestinal smooth muscle but not smooth muscle strips. May have a role in cardio-renal homeostasis through regulation of natriuresis and vasodilation. In vivo promotes natriuresis. In vitro, selectively vasodilates intestinal and vascular smooth muscle strips. May have a role in cardio-renal homeostasis through regulation of natriuresis and vasodilation. In vivo promotes natriuresis. In vitro, selectively vasodilates intestinal smooth muscle but not vascular smooth muscle strips. Homodimer; disulfide-linked antiparallel dimer. Detected in blood. Detected in blood. Detected in blood. Detected in urine. Not detected in blood. Increased electrolytes, osmolality and intracellular cAMP levels increase peptide secretion/excretion. Detected in blood. Detected in urine in one study. However, in another study, was not detected in urine. Detected in cytoplasmic bodies and neuronal processes of pyramidal neurons (layers II-VI) (By similarity). Increased secretion in response to the vasopressin AVP (By similarity). Likely to be secreted in response to an increase in atrial pressure or atrial stretch. In kidney cells, secretion increases in response to activated guanylyl cyclases and increased intracellular cAMP levels. Plasma levels increase 15 minutes after a high-salt meal, and decrease back to normal plasma levels 1 hr later (By similarity). Detected in blood. Slight increase in secretion in response to the vasopressin AVP. The precursor molecule is proteolytically cleaved by CORIN at Arg-122 to produce the atrial natriuretic peptide (By similarity). Undergoes further proteolytic cleavage by unknown proteases to give rise to long-acting natriuretic peptide, vessel dilator and kaliuretic peptide (By similarity). Additional processing gives rise to the auriculin and atriopeptin peptides (By similarity). In the kidneys, alternative processing by an unknown protease results in the peptide urodilatin (By similarity). Cleavage by MME initiates degradation of the factor and thereby regulates its activity. Degradation by IDE results in reduced activation of NPR1 (in vitro). During IDE degradation, the resulting products can temporarily stimulate NPR2 to produce cGMP, before the fragments are completely degraded and inactivated by IDE (in vitro). Degraded by IDE. Phosphorylation on Ser-128 decreases vasorelaxant activity. Belongs to the natriuretic peptide family. Results concerning the involvement of this peptide in blood volume and blood pressure homeostasis are conflicting. Several studies utilising in vitro and heterologous expression systems show that it is able to activate cGMP and promote vasodilation and natriuresis (By similarity). However, an in vivo study in rat found that it is not sufficient to induce any diuretic, natriuretic, nor hypotensive responses, and is unable to bind NPR1 nor increase guanylyl cyclase activity (By similarity). Results concerning the involvement of this peptide in blood volume and blood pressure homeostasis are conflicting. Several studies utilising in vitro and heterologous expression systems show that it is able to activate cGMP and promote vasodilation and natriuresis (By similarity). However, a heterologous and in vivo expression study in rat found that it is not sufficient to induce any diuretic, natriuretic, nor hypotensive responses, and is unable to bind NPR1 nor increase guanylyl cyclase activity (By similarity).