Interaction between atrial natriuretic peptide and renin angiotensin aldosterone system: endogenous antagonists

Article Abstract:

The enzyme renin is produced by the kidneys. Renin converts the blood protein angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasopressor, in that it constricts blood vessels, and also increases the production and release of the mineralocorticoid hormone aldosterone from the adrenal glands. Aldosterone causes sodium retention. Atrial natriuretic peptide (ANP) is a hormone released from the atria of the heart in response to an increase in blood pressure. ANP causes effects opposite to those of the renin-angiotensin system; ANP produces dilation of blood vessels, suppression of aldosterone, and increased excretion of water and sodium. Receptors or specific bindings sites for both ANP and angiotensin II are present on membranes in the brain, adrenal glands, blood vessels, and kidneys. In many physiologic situations, such as changes in body position, immersion in water, and high altitude, the blood levels of ANP and angiotensin II change inversely; in other words, if ANP levels increase, angiotensin II levels decrease and vice versa. Congestive heart failure (the inability of the heart to maintain circulation, characterized by accumulation of fluid in the lungs) and aging are conditions associated with high levels of ANP and decreased levels of renin and aldosterone. ANP may be the natural antagonist of the renin-angiotensin-aldosterone system; these two opposing systems may function to maintain the balance of blood pressure. (Consumer Summary produced by Reliance Medical Information, Inc.)

Laws, regulations and rules, Blood pressure

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Atrial natriuretic peptide in the recovery from high-output congestive heart failure

Article Abstract:

Large arteriovenous fistulas (AVF), abnormal tube-like passages between an artery and vein, increase the amount of blood returning to the heart, the pressure on the heart at the end of the relaxation phase of the heart cycle, and the volume of blood pumped out by the heart. These changes may lead to congestive heart failure, the inability of the heart to pump blood, which results in the accumulation of fluid within the lungs, and consequent retention of fluid and sodium. Closing the fistula eliminates the fluid and sodium and improves the symptoms associated with congestive heart failure. The mechanism underlying this response is not known. The role of atrial natriuretic peptide (ANP) in the elimination of sodium after closure of the fistula was examined. ANP is a hormone secreted by the atrial tissue in response to an increase in blood pressure. This hormone regulates blood pressure, blood volume, and cardiac output, and increases the excretion of salt. Two cases are described of elderly patients with AVF, signs of congestive heart failure, and elevated ANP levels, who underwent surgery to repair the fistula. One patient recovered and his ANP levels dropped to normal, whereas the other patient did not recover from surgery and died. Two other younger patients with small AVF had no signs of heart failure and had normal ANP levels. Thus, ANP may contribute to recovery from congestive heart failure resulting from AVF by enhancing sodium and water excretion. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Congestive heart failure, Fistula, Arteriovenous, Arteriovenous fistula

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Angiotensin-converting enzyme inhibition versus blockade of the renin-angiotensin system

Article Abstract:

The enzyme renin is produced by the kidneys. Renin converts the blood protein angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasopressor, in that it constricts blood vessels, and also increases the production and release of the mineralocorticoid hormone aldosterone from the adrenal glands. Aldosterone controls the metabolism of sodium, chloride, and potassium. Agents which prevent the action of ACE and the formation of angiotensin II have been used to treat hypertension, or abnormally high blood pressure. Studies have shown that there is a delay between the inhibition of angiotensin-converting enzyme by ACE inhibitors and reduction in angiotensin II levels, which reflect suppression of the renin-angiotensin system. In addition, because renin release by the kidneys is activated by low blood pressure, the lowering of blood pressure by ACE inhibitors causes an increase in renin and the subsequent increase in angiotensin I. This compensatory increase in renin in response to ACE inhibition is a major factor influencing the extent and duration of blockade of the renin-angiotensin system by ACE inhibitors. A better understanding of the relation between renin levels and ACE inhibitors may be useful in determining the duration of action and effective dose of ACE inhibitors. (Consumer Summary produced by Reliance Medical Information, Inc.)

ACE inhibitors, Angiotensin converting enzyme inhibitors, Renin

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