natriuresis

The discharge of sodium through urine is known as "natriuresis".

There are three naturally occurring protein hormones in the body that cause natriuresis.

The long term effect of antihypertensive drugs comes from their effects on the pressure natriuresis curve.

Bradykinin also causes natriuresis, contributing to a drop in blood pressure.

These can be used in patients undergoing diuretic therapy, since diuretics induce a natriuresis.

Excess natriuresis can be caused by:

Both drugs increased diuresis and natriuresis - effects that are thought to be due to the activation of renal D receptors.

Also, regulatory mechanisms such as increased natriuresis may counteract the effect of ACE on peripheral resistance.

This volume expansion and natriuresis was performed to increase renal blood flow and enhance calcium excretion.

Nesiritide promotes diuresis and natriuresis, thereby ameliorating volume overload.

Dopamine signaling affects diuresis and natriuresis.

It is localized in the kidney where it results in natriuresis upon binding to natriuretic peptides.

In the kidney it is inhibited by atrial natriuretic peptide, causing natriuresis and diuresis.

Natriuretic peptide refers to a peptide which induces natriuresis (the discharge of sodium through urine).

Although the ability for caffeine and theophylline to induce diuresis and natriuresis is well established, the mechanisms behind them are not well understood.

When administered intravenously, URO induces strong diuresis and natriuresis with tolerable hemodynamic side effects.

By impairing Na transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss.

Escape from the sodium-retaining effects of excess aldosterone (or other mineralocorticoids) in primary hyperaldosteronism, manifested by volume and/or pressure natriuresis.

Hypercalcemia causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the calcium sensing receptor (CaR).

It is also reported that this form of calcium increases renal plasma flow, diuresis, natriuresis, glomerular filtration rate, and prostaglandin E2 and F1-alpha levels.

Also, elevated levels of progesterone potently reduce the sodium-retaining activity of aldosterone, resulting in natriuresis and a reduction in extracellular fluid volume.

In Liddle's Syndrome NEDD4 is unable to bind to the ENaC and uncontrolled Natriuresis occurs.

NEP inhibition results in elevated natriuretic peptide levels, promoting natriuresis, diuresis, vasodilation, and reductions in preload and ventricular remodeling.

Dopamine induces natriuresis (sodium loss) in the kidneys, and has a diuretic effect, potentially increasing urine output from 5 ml/kg/hr to 10 ml/kg/hr.

Natriuresis is similar to diuresis, the excretion of an unusually large quantity of urine, except that in natriuresis the urine is exceptionally salty.