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Sodium ions, aldosterone

Triamterene is a pyrazine derivative that inhibits reabsorption of sodium ions without increasing excretion of potassium ions. It exhibits the same approximate effect as spironolactone however, it does not competitively bind with aldosterone receptors. Its action does not have an effect on secretion of aldosterone or its antagonists, which are a result of direct action on renal tubules. [Pg.291]

Amyloride is also a potassium sparing diuretic that exhibits moderate activity. It is not an antagonist of aldosterone. It inhibits reabsorption of sodium ions and reduces excretion of... [Pg.291]

Reduction in plasma volume secondary to the enhanced excretion of sodium ions and water and the regression of edema, if present. These effects are accompanied by a reduction in cardiac preload. During long-term treatment most of these effects are counteracted by various regulatory mechanisms, such as a persistent rise in plasma renin and aldosterone. [Pg.342]

Adrenocorticoid hormones are produced in the adrenal glands. They regulate a variety of metaholic processes. The most important mineralo-corticoid is aldosterone, an aldehyde as well as a ketone, which regulates the reahsorption of sodium and chloride ions in the kidney, and increases the loss of potassium ions. Aldosterone is secreted when hlood sodium ion levels are too low to cause the kidney to retain sodium ions. If sodium levels are elevated, aldosterone is not secreted, so some sodium will he lost in the urine and water. Aldosterone also controls swelling in the tissues. [Pg.359]

Figure 12.6 Mechanism of action of mineralocortjcoid receptor antagonists in the collecting tubule. Aldosterone enters the tubular cell by the basolateral surface and binds to a specific mineralocorticoid receptor (MNR) in the cytoplasm. The hormone receptor complex triggers the production of an aldosterone-induced protein (AlP) by the cell nucleus (NUC). The AIP acts on the sodium ion channel (ic) to augment the transport of Na+across the basolateral membrane and in to the cell. An increase in AIP activity leads to the recruitment of dormant sodium ion channels and Na pumps (P) in the cell membrane. AIP also leads to the synthesis of new channels and pumps within the cell. The increase in Na+conductance causes electrical changes in the luminal membrane that favour the excretion of intracellular cations, such as K+and H-h. Spironolactone competes with aldosterone for the binding site on the MNR and forms a complex which does not excite the production of AIP by the nucleus. Figure 12.6 Mechanism of action of mineralocortjcoid receptor antagonists in the collecting tubule. Aldosterone enters the tubular cell by the basolateral surface and binds to a specific mineralocorticoid receptor (MNR) in the cytoplasm. The hormone receptor complex triggers the production of an aldosterone-induced protein (AlP) by the cell nucleus (NUC). The AIP acts on the sodium ion channel (ic) to augment the transport of Na+across the basolateral membrane and in to the cell. An increase in AIP activity leads to the recruitment of dormant sodium ion channels and Na pumps (P) in the cell membrane. AIP also leads to the synthesis of new channels and pumps within the cell. The increase in Na+conductance causes electrical changes in the luminal membrane that favour the excretion of intracellular cations, such as K+and H-h. Spironolactone competes with aldosterone for the binding site on the MNR and forms a complex which does not excite the production of AIP by the nucleus.
Aldosterone, which is classified as a mineralo-corticoid, is produced under the control of the renin-angiotensin hormone system (Box 22-D), which is stimulated when sodium ion receptors in the kidneys... [Pg.1254]

Aldosterone enhances the reabsorption of sodium ions in the kidneys, thus compensating for their loss in the sweat. [Pg.86]

Sodium ions are controlled in a homeostatic process involving aldosterone which increases sodium ion absorption in the distal convoluted tubules. [Pg.368]

Aldosterone stimulates an increase in the reabsorption of sodium ions from the kidney tubules which causes an increase in the volume of water that is reabsorbed from the tubule. This increase in water reabsorption increases the volume of blood, which ultimately raises the blood pressure. [Pg.368]

In the distal tubule (site 4), sodium ions are exchanged for potassium and hydrogen ions. The sodium ions are transported across the epithelial Na chaimel (called ENaC), which is stimulated by aldosterone. The aldosterone (mineralocorticoid)... [Pg.530]

B. Aldosterone causes resorption of sodium ions and, consequently, the resorption of water. Vasopressin (antidiuretic hormone) causes water resorption. [Pg.319]

The major effect is on the distal tubules of nephrons, where aldosterone promotes sodium retention and potassium excretion. Under the influence of aldosterone, sodium ions are actively transported out of the distal tubular cell into blood, and this transport is coupled to passive potassium flux in the opposite direction. Consequently, intracellular [Na" ] is diminished and intracellular [K+] is elevated. This intracellular diminution of [Na+] promotes the diffusion of sodium from the filtrate into the cell, and potassium diffuses into the filtrate. Aldosterone also stimulates sodium reabsorption from salivary fluid in the salivary gland and from luminal fluid in the intestines, but these sodium-conserving actions are of minor importance. [Pg.755]

Aldosterone is a steroid hormone produced by the adrenal cortex and secreted into the bloodstream when blood sodium ion levels are too low. Upon reaching its target tissues in the kidney, aldosterone activates a set of reactions that cause sodium ions and water to be returned to the blood. If sodium levels are elevated, aldosterone is not secreted from the adrenal cortex and the sodium ions filtered out of the blood by the kidney will be excreted. [Pg.538]

Aldosterone decreases urinary sodium excretion by increasing sodium reabsorption in the renal tubules at the expense of potassium and hydrogen ions. Aldosterone also stimulates sodium conservation by the sweat glands and the... [Pg.80]

Candesartan is an antihypertensive combination. Candesartan antagonizes the effect of angiotensin II (vasoconstriction and aldosterone secretion) by blocking the angiotensin II receptor (AT receptor) in vascular smooth muscle and the adrenal gland, producing decreased BE. Hydrochlorothiazide (HCTZ) increases chloride, sodium, and water excretion by interfering with hansport of sodium ions across renal tubular epithelium. [Pg.128]

Mineralocorticoids such as aldosterone are also synthesized in the adrenal cortex and are secreted in response to angiotensin II or III, rising potassium levels in the blood, or hyponatremia (low levels of sodium ions in the blood). Aldosterone stimulates sodium reuptake in the kidney, sweat glands, salivary glands, and other... [Pg.643]


See other pages where Sodium ions, aldosterone is mentioned: [Pg.203]    [Pg.208]    [Pg.156]    [Pg.322]    [Pg.290]    [Pg.208]    [Pg.156]    [Pg.1254]    [Pg.402]    [Pg.83]    [Pg.707]    [Pg.708]    [Pg.707]    [Pg.708]    [Pg.23]    [Pg.167]    [Pg.1479]    [Pg.156]    [Pg.608]    [Pg.341]    [Pg.117]    [Pg.320]    [Pg.253]    [Pg.1100]    [Pg.1110]    [Pg.1110]    [Pg.258]    [Pg.153]    [Pg.481]    [Pg.121]   
See also in sourсe #XX -- [ Pg.94 ]




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