It is associated with accumulation of atrial natriuretic factor.

Similarly, this review will not discuss any of the yet experimental agents such as atrial natriuretic factor.

It is known by several names including auriculin, atriopeptin and atrial natriuretic factor.

There are three distinct atrial natriuretic factor receptors identified so far in mammals: natriuretic peptide receptors 1, 2, and 3.

Many vasoactive chemicals have been hypothesized as being involved in mediating the systemic hemodynamic changes, including atrial natriuretic factor, prostacyclin, thromboxane A2, and endotoxin.

Theoretical concerns surround the role of the LAA in thirst regulation and water retention because it is an important source of atrial natriuretic factor.

It is an antisense transcript of the NPPA gene, which encodes the precursor of cardiodilatin-related peptide and atrial natriuretic factor.

They also contain neurons with receptors for angiotensin, atrial natriuretic factor, endothelin and relaxin, each of which is important in the regulation of fluid and electrolyte balance.

A stimulant, atrial natriuretic factor (ANF) increases cGMP production in the kidneys, which increases function of the glomerulus by a combination of relaxing and contracting arterioles.

Examples are: Aβ, IAPP, Atrial natriuretic factor (in isolated atrial amyloidosis) and Calcitonin (in medullary carcinoma of the thyroid)

In turn, peptide hormones such as the atrial natriuretic factor activate membrane-bound GC, while soluble GC is typically activated by nitric oxide to stimulate cGMP synthesis.

Inhibitors have been designed with the aim of developing analgesic and antihypertensive agents that act by preventing neprilysin's activity against signaling peptides such as enkephalins, substance P, endothelin, and atrial natriuretic factor.

BNP binds to and activates the atrial natriuretic factor receptors NPRA, and to a lesser extent NPRB, in a fashion similar to atrial natriuretic peptide (ANP) but with 10-fold lower affinity.

TGFbeta mediated activation of p38 MAPK decreases KLF15 permitting the upreg of myocardin and stimulate the expression of serum response factor target genes, such as atrial natriuretic factor eventually leading to left ventricular hypertrophy which often progresses to heart failure.