Disease relevance of Salt Gland

• Since the initial inositol phosphate production upon receptor activation with carbachol and the resulting calcium signals were not affected by pertussis toxin-pretreatment of salt gland cells, we conclude that muscarinic receptors are coupled to phospholipase C by a Gq-type G protein [1].
• Adaptive hypertrophy of the nasal salt glands was not steroid-dependent since there was no measurable decrease in the weight of the glands during a 2-week period following adrenalectomy [2].

High impact information on Salt Gland

• In rectal glands perfused under basal conditions without secretagogues, Cl- secretion was 151+/-65 microeq/h/g. Vasoactive intestinal peptide (VIP), forskolin, and genistein led to 10-, 6-, and 4-fold increases in Cl- secretion [3].
• To investigate whether acute hormonal stimulation of chloride secretion is coupled to the trafficking of CFTR, we used the intact shark rectal gland, a model tissue in which salt secretion is dynamically regulated and both chloride secretion and cellular CFTR immunofluorescence can be quantified in parallel [3].
• Endogenous adenosine is an autacoid feedback inhibitor of chloride transport in the shark rectal gland [4].
• Characterization of muscarinic acetylcholine receptors in the avian salt gland [5].
• In addition, the loop diuretic furosemide, which interferes with ion transport processes in the salt gland, competitively inhibits [3H]QNB binding [5].

Biological context of Salt Gland

• Carbachol-stimulated phosphorylation of the Na-K-Cl cotransporter of avian salt gland. Requirement for Ca2+ and PKC Activation [6].
• Sodium- and potassium-activated adenosine triphosphatase of the nasal salt gland of the duck (Anas platyrhynchos). Purification, characterization, and NH2-terminal amino acid sequence of the phosphorylating polypeptide [7].
• Ouabain binding during plasma membrane biogenesis in duck salt gland [8].
• Treatment of ducks drinking fresh water with large doses of corticosterone and mammalian ACTH for 48 hr had no significant effects on salt-gland weight, RNA or DNA; mammalian prolactin treatment for 48 hr significantly raised [RNA] [9].
• Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells [10].

Anatomical context of Salt Gland

• Basolateral plasma membrane localiztion of ouabain-sensitive sodium transport sites in the secretory epithelium of the avian salt gland [11].
• The release of all the sialic acid from the electric organ enzyme and the release of 40% of the sialic acid from the rectal gland enzyme did not affect (sodium + potassium)-activated adenosine triphosphatase activity [12].
• Immunoblots and Coomassie Blue-stained companion gels showed double species of the 100-kDa subunit in sucrose gradient fractions of mouse brain and kidney, bovine grey and white matter, purified lamb kidney and duck salt gland holoenzyme, electroplax microsomes, and NaI-extracted microsomes of goldfish and rat brain [13].
• The composition of the rectal gland fluid suggests that its epithelial cells are permeable to water and not to urea [14].
• These results indicate that the rectal gland maintains a selective barrier to urea in its basolateral membranes [14].

Associations of Salt Gland with chemical compounds

• The present studies define the physiologic role of endogenous adenosine in the perfused shark rectal gland, a model epithelia for hormone-stimulated chloride transport [4].
• In this study, these receptors were characterized and quantitated in homogenates of salt gland from domestic ducks adapted to conditions of low (freshwater, FW) and high (saltwater, SW) salt stress using the cholinergic antagonist [3H]-quinuclidinyl benzilate (QNB) [5].
• Na+,K(+)-ATPase from the salt gland of Squalus acanthias was solubilized in a polyoxyethylene ether detergent, octa(ethylene glycol) dodecyl monoether [15].
• The results demonstrate both B creatine kinase and mitochondrial creatine kinase proteins are present in the rectal gland, an isoform composition which is the same as in the mammalian kidney [16].
• Effects of lipophilic ions, tetraphenylphosphonium (TPP+) and tetraphenylboron (TPB-), on interactions of Na+ and K+ with Na,K-ATPase were studied with membrane-bound enzyme from bovine brain, pig kidney, and shark rectal gland [17].

Gene context of Salt Gland

• Neuropeptide Y inhibits chloride secretion in the shark rectal gland [18].
• The inhibitory action of NPY was not prevented by procaine, nifedipine, or diltiazem, suggesting that it was not secondary to the release of somatostatin or other unknown neurotransmitters from rectal gland nerves [18].
• We have examined the xenobiotic transport function of a putative multidrug resistance associated protein, MRP2, in three different epithelia: the insect renal (Malpighian) tubules, the secretory tubule of the shark rectal gland, and in ductules of the human breast [19].
• Identification of a phospholemman-like protein from shark rectal glands. Evidence for indirect regulation of Na,K-ATPase by protein kinase c via a novel member of the FXYDY family [20].
• These results indicate that shark rectal gland transport on MRP2 is regulated by ET acting through an ET(B) receptor and PKC [21].

Analytical, diagnostic and therapeutic context of Salt Gland

• Immunoprecipitation of pp170 from salt gland cells resulted in the selective extraction of a single protein whose phosphorylation state was increased approximately 5-fold in response to carbachol or VIP [22].
• Circulatory and osmoregulatory effects of angiotensin II perfusion of the third ventricle in a bird with salt glands [23].
• Analogous experiments performed with enzyme from shark rectal gland showed similar effects, but with a significantly lower amplitude of the fluorescence change and a higher saturating value of 1/tau for both the NaCl and choline chloride titrations [24].
• By employing the perforated patch-clamp whole-cell recording technique we investigated the effects of VIP on membrane potential and transmembrane currents in avian exocrine salt gland cells [25].
• We measured the venous and arterial pressure, as well as the rate of secretion and content of cyclic AMP and high energy phosphate compounds, of the rectal gland of the anaesthetized dogfish, Squalus acanthias (L.). Intravenous infusion of isotonic solutions produced a very large increase in the rate of secretion by the rectal gland [26].

References