Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Review of 18th and 19th century psychiatric therapies raises the possibility that several may have altered the activity of vasopressin or Na-K-ATPase. Bleeding, whirling, nausea created by medicines, and vagus nerve stimulation by application of electricity through the skin all perturb the hypothalamic hormone, arginine vasopressin, while helleborus and digitalis inhibit the sodium pump enzyme, Na-K-ATPase. These approaches were used with reported benefit many years ago, acting on the brain in ways ongoing research suggests may play a role in affective disorders. Study of long-abandoned treatments may clarify their mechanisms of action and the characteristics of responsive patients.
 ...
PMID:Did some 18th and 19th century treatments for mental disorders act on the brain? 1496 30

Nephrotic edema are the clinical feature of isolated interstitial expansion. Expanded interstitial compartment compensates sodium accumulation in the extracellular volume due to inappropriate renal sodium retention. Renal sodium retention is brought about by an activation of the molecular structures responsible for the reabsorption of sodium along the cortical collecting duct: amiloride-sensitive epithelial sodium channel at the apical face and sodium pump at the basolateral face of the principal cell. This activation is independent of aldosterone and vasopressin. The asymmetry of expansion between interstitium and plasma compartments is due to impaired Starling forces and increased fluid transfer through the capillary wall. The lack of significant changes in transcapillary oncotic and hydrostatic gradients suggests that increased hydraulic conductivity due to transconformation of endothelial intercellular junctions drives the leakage of fluid into the interstitium and allows to understand the mobility of nephrotic edema. Consistently with the site of renal sodium retention and the activation of the epithelial sodium channel, the association of amiloride and furosemide is efficient to increase urinary sodium excretion, to reverse sodium balance and to remove edema from patients with nephrotic syndrome.
 ...
PMID:[Molecular mechanism of edema formation in nephrotic syndrome]. 1535 Oct

The collecting duct of normal kidney exhibits significant activity of the MEK1/2-ERK1/2 pathway as shown in vivo by immunostaining of phosphorylated active ERK1/2 (pERK1/2). The MEK1/2-ERK1/2 pathway controls many different ion transports both in proximal and distal nephron, raising the question of whether this pathway is involved in the basal and/or hormone-dependent transepithelial sodium reabsorption in the principal cell of the cortical collecting duct (CCD), a process mediated by the apical epithelial sodium channel and the basolateral sodium pump (Na,K-ATPase). To answer this question we used ex vivo microdissected CCDs from normal mouse kidney or in vitro cultured mpkCCDcl4 principal cells. Significant basal levels of pERK1/2 were observed ex vivo and in vitro. Aldosterone and vasopressin, known to up-regulate sodium reabsorption in CCDs, did not change ERK1/2 activity either ex vivo or in vitro. Basal and aldosterone- or vasopressin-stimulated sodium transport was down-regulated by the MEK1/2 inhibitor PD98059, in parallel with a decrease in pERK1/2 in vitro. The activity of Na,K-ATPase but not that of epithelial sodium channel was inhibited by MEK1/2 inhibitors in both unstimulated and aldosterone- or vasopressin-stimulated CCDs in vitro. Cell surface biotinylation showed that intrinsic activity rather than cell surface expression of Na,K-ATPase was controlled by pERK1/2. PD98059 also significantly inhibited the activity of Na,K-ATPase ex vivo. Our data demonstrate that the ERK1/2 pathway controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell and indicate that basal constitutive activity of the ERK1/2 pathway is a critical component of this control.
 ...
PMID:ERK1/2 controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell of the cortical collecting duct of the mouse kidney. 1545 67

In the kidney, the collecting duct (CD) is the site of final Na+ reabsorption, according to Na+ balance requirements. In this segment of the renal tubule, principal cells may reabsorb up to 5% of the filtered sodium. The driving force for this process is provided by the basolateral Na,K-adenosine triphosphatase (ATPase) (sodium pump). Na,K-ATPase activity and expression in the CD are modulated physiologically by hormones (aldosterone, vasopressin, and insulin) and nonhormonal factors including intracellular [Na+] and extracellular osmolality. In this article, we review the short- and long-term hormonal regulation of Na,K-ATPase in CD principal cells, and we analyze the integrated network of implicated signaling pathways with an emphasis on the latest findings.
 ...
PMID:Hormonal and nonhormonal mechanisms of regulation of the NA,K-pump in collecting duct principal cells. 1613 86

Life is maintained in a sea water-like internal environment. The homeostasis of this environment is dependent on osmosensory system translation of hydromineral information into osmotic regulatory machinery at system, tissue and cell levels. In the osmosensation, hydromineral information can be converted into cellular reactions through osmoreceptors, which changes thirst and drinking, secretion of antidiuretic vasopressin (VP), reabsorption of water and salt in the kidneys at systemic level as well as cellular metabolic activity and survival status at tissue level. The key feature of osmosensation is the activation of mechanoreceptors or mechanosensors, particularly transient receptor potential vallinoid (TRPV) and canonical (TRPC) family channels, which increases cytosolic Ca2+ levels, activates osmosensory cells including VP neurons and triggers a series of secondary reactions. TRPV channels are sensitive to both hyperosmotic and hyposmotic stimuli while TRPC channels are more sensitive to hyposmotic challenge in neurons. The activation of TRP channels relies on changes in cell volume, membrane stretch and cytoskeletal reorganization as well as hydration status of extracellular matrix (ECM) and activity of integrins. Different families of TRP channels could be activated differently in response to hyperosmotic and hyposmotic stimuli in different spatiotemporal orders, leading to differential reactions of osmosensory cells. Together, they constitute the osmosensory machinery. The activation of this osmoreceptor complex is also associated with the activity of other osmolarity-regulating organelles, such as water channel protein aquaporins, Na-K-2Cl cotransporters, volume-sensitive anion channels, sodium pump and purinergic receptors in addition to intercellular interactions, typically astrocytic neuronal interactions. In this article, we review our current understandings of the composition of osmoreceptors and the processes of osmosensation.
 ...
PMID:Interactions of the Mechanosensitive Channels with Extracellular Matrix, Integrins, and Cytoskeletal Network in Osmosensation. 2842 87


<< Previous 1 2