renin-angiotensin-aldosterone system , RAA system (Abkürzung) , RAAS (Abkürzung)

Changes in blood pressure and activity of the renin-angiotensin-aldosterone system may contribute to these different effects.

If the renin-angiotensin-aldosterone system is abnormally active, blood pressure will be too high.

It is believed to exert its antihypertensive effect through the renin-angiotensin-aldosterone system.

Aldosterone production is suppressed by captopril through the renin-angiotensin-aldosterone system.

Secretion of renin, which is a key part of the renin-angiotensin-aldosterone system.

Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system.

Renin, the first enzyme in the renin-angiotensin-aldosterone system, plays a role in blood pressure control.

This apparatus controls blood pressure through the Renin-Angiotensin-Aldosterone system.

Part of the renin-angiotensin-aldosterone system, renin is an enzyme involved in the regulation of aldosterone levels.

This allowed for a potent carboxypeptidase A inhibitor to be used to inhibit the enzyme and, thus, lower blood pressure through the renin-angiotensin-aldosterone system.

Inhibits renin secretion, thereby inhibiting the renin-angiotensin-aldosterone system.

Another system maintaining the extracellular fluid volume, peripheral resistance and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system.

Enalapril as a treatment for high blood pressure works by modulating the renin-angiotensin-aldosterone system (RAAS).

These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin-angiotensin-aldosterone system.

The release of renin is an essential component of the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and volume.

Low renal blood flow activates the renin-angiotensin-aldosterone system (RAAS), causing fluid retention and mild hypertension.

The renin-angiotensin-aldosterone system (RAAS) plays a key role in the pathology of cardiovascular disease, hypertension, diabetic kidney disease and heart failure.

As such it has potent antimineralocorticoid properties, counteracts the estrogen-stimulated activity of the renin-angiotensin-aldosterone system, and has also been shown to possess mild antiandrogen activity.

Treatment for the SNP associated hyperreninemia involves drugs to block the Renin-Angiotensin-Aldosterone system to relieve the aforementioned stresses on the heart.

Decreased output of blood by the left ventricle causes the body to compensate by increasing sympathetic tone and activating the renin-angiotensin-aldosterone system (RAAS).

A possible short term reduction of microalbuminuria due to hydrochlorothiazide's hypotensive effect may have been progressively counterbalanced by the effective renin-angiotensin-aldosterone system stimulation provoked by the same drug.

If a standard drug treatment is found to dangerously inhibit the renin-angiotensin-aldosterone system, it can be withdrawn and the effects reversed quickly, but that would not be true of the vaccine.

Angiotensin-converting enzyme ACE, aminopetidase A and aminopeptidase N have cascading actions in the renin-angiotensin-aldosterone system, which suggests a common phylogenetic origin between these molecules.

When angiotensin II levels are increased due to activation of the renin-angiotensin-aldosterone system, most of the arteries in the body experience vasoconstriction, in order to maintain adequate blood pressure.

Hyperactivity of the renin-angiotensin-aldosterone system is manifested by hypertension with hypervolemia which is severe and not responsive (or minimally responsive) to medications/lifestyle modifications that would usually control essential hypertension.