Atrial natriuretic peptide (CDD/ANP-99-126) is a hormone system of clinical importance.<unk>  (CDD/ ANP-95-126) is a homologue natriuretic peptide that differs from CDD/ANP-99-126, which is excreted into the circulation via exocytosis. The prototype of the natriuretic hormones is cardiodilatin / atrial natriuretic peptide (CDD/ANP). The endocrine heart is composed of specific myoendocrine cells that synthesize and secrete the natriuretic peptide hormones, which exhibit diuretic and vasorelaxant properties; secretion is the basis for a paracrine system regulating water and sodium reabsorption. Research efforts since the early 1980s have studied their effects on electrolyte homeostasis. When administered intravenously,<unk>  induces strong diuresis and natriuresis with tolerable hemodynamic side effects.<unk>  is localized in the kidney, differentially processed (involved in the regulation of body fluid volume and water-electrolyte excretion, while circulating), and secreted into the urine. As a consequence,<unk>  is involved in drug development along with the prohormone CDD/ANP-1-126 and cardiodilatin CDD/ANP-99-126. A message for the preprohormone is transcribed in the heart and kidneys from the gene of NP type A, resulting in a cGMP-dependent signal transduction, which induces diuresis and natriuresis, differentially processed to a peptide of 32 amino acids from the same precursor as renal ANP, may not be identical to the circulating cardiac hormone ANP. The kidneys produce their own natriuretic 32-residue peptide.<unk>  renal natriuretic peptide potency equals or exceeds that of Atriopeptin ANP-(99-126), the prototype of cardiodilatin. Atriopeptin is only of trivial importance in the regulation of sodium excretion during normal living conditions.<unk>  is little affected by renal enzymes that inactivate atriopeptin, as the kidney elutes with<unk>  rather than with ANP. The degradation rates of (125I)-urodilatin and 125I-ANP by pure recombinant NEP (rNEP) were compared. Phosphoramidon, a potent inhibitor of NEP, completely protected both peptides from metabolism by rNEP.<unk>  has a four-residue extension at the N-terminus neutral endopeptidase-24.11 (NEP) plays a physiological role in metabolizing atrial natriuretic peptide, and C-type natriuretic peptide (prohormone) degraded the bioactive peptides at about half the rate though the C-terminal that compete with natriuretic peptides for hydrolysis by neutral endopeptidase.
Urodilatin
Cortistatin 
Sertaconazole
Nystatin
Ketoconazole
Levoketoconazole
Itraconazole
Terbinafine