Collecting duct

4d Collecting Duct. The collecting tubule and duct performs final regulation and fine-tuning of urinary volume and composition. Active transport systems in the collecting tubule reabsorb Na+ and secrete K+ and H+. Additionally, the 

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Spironolactone antagonizes the effects of aldosterone by binding at the aldosterone receptor in the cytosol of the late distal tubules and renal collecting ducts. Side effects of spironolactone are gynecomastia, decreased Hbido, and impotency. 

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). 

Problems can arise if several cupboards, each with its own fan, are connected to a single common duct and discharge stack. If a fume cupboard was switched off or a fan failed, flow through the cupboard could be reversed causing contaminants to be discharged into the room. The collecting duct should be kept at a lower pressure by its own fan to reduce this risk. 

AQP6 is expressed in the intercalated cells of the kidney collecting duct. This channel is hardly permeable to water, but capable of transporting anions, including chloride, and is therefore thought to play a role in maintenance of body acid-base balance or in intracellular vesicle acidification. 

Inhibition of V2 vasopressin receptors causes an increase in urine volume primarily by reducing the re-absoiption of water along the collecting duct, an aquaretic effect that is fundamentally different from the natriuretic actions discussed so far. Nevertheless, some of the conditions calling for the use of natriuretic intervention are identical to those in which the administration of a new class of orally active nonpeptide V2 antagonists may be useful (tolvaptan, lixivaptan, and others). 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

Til tee successive tubule portions contribute to the ASDN the late portion of the distal convoluted tubule, the connecting tubule, and the collecting duct. The recent observation that collecting duct-specific inactivation of aENaC in the mouse kidney does not impair sodium and potassium balance, suggests that the more proximal nephron segments (late distal convoluted tubule, connecting tubule) are mainly important for-achieving sodium and potassium balance. 

Urodilatin is a peptide similar to atrial natriuretic peptide, which is produced in the distal tubule of the kidney and promotes sodium excretion and diuresis by acting on receptors localized on the luminal site of the collecting duct of the nephron. 

The V2R is expressed in collecting duct cells in rodents it is also expressed in cells of the thick ascending limb of Henle s loop (TAL). V2R-induced Gs-mediated activation of AC, the subsequent increase... 

The VACM-1 receptor is a membrane-associated protein with a single putative transmembrane domain that binds selectively AVP (XD — 2 nM), but cannot discriminate between VXR and V2R analogues. It is expressed in endothelial and medullary collecting duct cells and upon stimulation by AVP. It induces a mobilization of cytosolic-free Ca2+, decreases cAMP production and inhibits cellular growth via MAPK phosphorylation and p53 expression. The mechanism of action and physiological functions of this new receptor are not well understood, but it seems to participate in the regulation of AVP induced signal transduction pathways or of a yet unidentified peptide. 

Large conductance CP-channels were described for renal epithelial cells such as MDCK-cells, urinary bladder, collecting duct and A6-cells [51-54] and in pulmonary alveolar cells [55]. 

Higher vasopressin concentrations are linked to dilutional hyponatremia and a poor prognosis in HF. Vasopressin exerts its effects through vasopressin type la (Vla) and vasopressin type 2 (V2) receptors.5,7 Vasopressin type la stimulation leads to vasoconstriction, while actions on the V2 receptor cause free water retention through aquaporin channels in the collecting duct. Vasopressin increases preload, afterload, and myocardial oxygen demand in the failing heart. 

The posterior pituitary is innervated by direct nervous stimulation from the hypothalamus, resulting in the release of specific hormones. The hypothalamus synthesizes two hormones, oxytocin and vasopressin. These hormones are stored in and released from the posterior pituitary lobe. Oxytocin exerts two actions (1) it promotes uterine contractions during labor, and (2) it contracts the smooth muscles in the breast to stimulate the release of milk from the mammary gland during lactation. Vasopressin is an antidiuretic hormone (ADH) essential for proper fluid and electrolyte balance in the body. Specifically, vasopressin increases the permeability of the distal convoluted tubules and collecting ducts of the nephrons to water. This causes the kidney to excrete less water in the urine. Consequently, the urine becomes more concentrated as water is conserved. 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Antidiuretic hormone promotes the reabsorption of water from the tubules of the kidney, or antidiuresis. Specifically, it acts on the collecting ducts and increases the number of water channels, which increases the diffusion coefficient for water. This results in the body s conservation of water and the production of a low volume of concentrated urine. The reabsorbed water affects plasma osmolarity and blood volume. This effect of ADH on the kidney occurs at relatively low concentrations. At higher concentrations, ADH causes constriction of arterioles, which serves to increase blood pressure. Antidiuretic hormone secretion is regulated by several factors ... 

More simply, in the early regions of the tubule (proximal tubule and Loop of Henle), Na+ ions leave the lumen and enter the tubular epithelial cells by way of passive facilitated transport mechanisms. The diffusion of Na+ ions is coupled with organic molecules or with other ions that electrically balance the flux of these positively charged ions. In the latter regions of the tubule (distal tubule and collecting duct), Na+ ions diffuse into the epithelial cells through Na+ channels. 

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