Index
It is a polypeptide with a vasodilator effect.
Natriuretic peptides are peptide hormones that are synthesized in the heart, brain, and other organs.
Atrial natriuretic peptide (ANP) is a 28 amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distention, angiotensin II, endothelin, and sympathetic (beta-adrenoceptor-mediated) stimulation.
Therefore, elevated levels of ANP are found during hypervolemic states (high blood volume) and congestive heart failure.
Brain-type natriuretic peptide (BNP; 32 amino acids), although first identified in the brain, is produced primarily by ventricular tissue in the heart, and like ANP, there is enhanced synthesis and release of BNP during failure cardiac.
Neutral endopeptidase (NEP) is a circulating enzyme that degrades natriuretic peptides. Therefore, inhibition of this enzyme increases circulating levels of natriuretic peptide and enhances its effects.
Other names for ANP:
- Type A natriuretic peptide.
- Factor natriurético atrial.
- Atriopeptin.
- Auriculin.
- Cardiodilatin.
- Natriodilatin
The term atrial, in ANP, refers to the atria, which are the two upper (and smaller) chambers of the heart. This is where ANP is manufactured, stored, and released primarily in people, especially in the right atrium.
Role of the ANP
Atrial natriuretic peptide (ANP) is a cardiac hormone that plays important roles in maintaining cardio-renal homeostasis. The peptide structure is highly conserved between species.
ANP plays a key role in regulating salt and water balance, as well as blood pressure homeostasis. Furthermore, ANP is involved in the pathophysiology of hypertension and heart failure, and exerts a cellular antiproliferative effect on the cardiovascular system.
More recently, the use of molecular genetic approaches has suggested a direct contributory role for ANP in the development of hypertension and cerebrovascular disorders.
Cardiovascular and kidney effects
Natriuretic peptides are involved in the long-term regulation of sodium and water balance, blood volume, and blood pressure.
These peptide hormones decrease the release of aldosterone by the adrenal cortex, increase the glomerular filtration rate (GFR) and filtration fraction, produce natriuresis and diuresis (potassium sparing), and decrease renin release, thereby decreasing the circulating levels of angiotensin II.
These actions contribute to a reduction in blood volume and therefore central venous pressure (CVP), pulmonary capillary wedge pressure, cardiac output, and arterial pressure.
Chronic elevations of ANP appear to lower arterial blood pressure primarily by decreasing systemic vascular resistance. The systemic vasodilation mechanism involves ANP receptor-mediated elevations in vascular smooth muscle cGMP as well as attenuating sympathetic vascular tone.
This latter mechanism may involve ANP acting on sites within the central nervous system, as well as through inhibition of norepinephrine release by sympathetic nerve endings.
In summary, natriuretic peptides serve as a counter-regulatory system for the renin-angiotensin-aldosterone system.
Therapeutic uses
Heart failure
Heart failure leads to activation of the renin-angiotensin-aldosterone system, which causes increased retention of sodium and water in the kidneys.
This, in turn, increases blood volume and contributes to elevated venous pressures associated with heart failure, which can lead to pulmonary and systemic edema. Increased angiotensin II also causes systemic vasoconstriction, which increases afterload in the left ventricle.
The primary use of a natriuretic in heart failure is to reduce congestion and pulmonary and / or systemic edema, and associated clinical symptoms (eg, shortness of breath, dyspnea).
Natriuretics can also reduce afterload on the heart by promoting systemic vasodilation, which can lead to better ventricular ejection.
specific drugs
Recombinant human BNP, or nesiritide, is approved for use in the acute treatment of decompensated congestive heart failure caused by systolic dysfunction.
As a peptide, nesiritide has poor bioavailability and is therefore only available for intravenous administration. With a short half-life of less than 20 minutes, it is administered as a continuous infusion after a bolus injection.
This drug is very effective in reducing pulmonary capillary wedge pressure and improving dyspnea in this patient population.
Adverse side effects and contraindications
The most common side effect of nesiritide is hypotension, which can last for a long time. Therefore, it is important to monitor blood pressure during drug administration.
Azotemia (an elevated level of urea in the blood or other nitrogen-containing compounds) can occur in patients with kidney disease in whom kidney function depends on the activated renin-angiotensin-aldosterone system.
This medicine should not be used in patients who have cardiogenic shock or who have systolic pressures less than 90 mmHg.
