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The human airway cell line Calu-3 with a serous phenotype was examined to determine the mechanics by which cyclic adenosine monophosphate (cAMP) activates the cystic fibrosis transmembrane conductance regulator chloride channel (CFTR Cl-) secretion. The findings confirmed the cAMP stimulation of CFTR channels localized in the apical plasma membrane. However, the recruitment of CFTR from an intracellular source prior to crossing the plasma membrane was ruled out. This implies the involvement of CFTR-mediated Cl- secretion in human airway epithelial serous cells in cystic fibrosis.

Mouse inner medullarity collecting duct cells (mIMCD-K2) were analyzed to determine the effects of hyperosmolality on electrogenic Na2+ adsorption (IsupNasubSC) and electrogenic Cl secretion (IsupClsubSC). Acute and chronic hyperosmolality in mIMCD-K2 cell lines reduced basal IsupNasubSc and IsupClsubSC due to elevations in NaCl and urea. Furthermore, the renal transport of urea, water, Na2+ and Cl- across IMCD were dependent on the osmolality of the interstitial fluid.

Expression of guanosine 3',5'-cyclic monophosphate (cGMP)-gated channels and alpha-messenger rat epithelial Na+ channel (alpha-mENaC) in nephrotic cells were analyzed by the localization of messenger ribonucleic acid (mRNA). Reverse transcription-polymerase chain reaction hybridization indicated the role of cGMP and alpha-mENaC in mediating the Na+ absorption of nephron segments. The mRNA that promotes cGMP-gated cation channel and alpha-mENaC is coexpressed at the medullary thick ascending limb, distal convoluted tubule, cortical collecting duct, outer and inner medullary collecting duct.

A study was conducted to determine if adenosine and adenosine A1 receptors are involved in the regulation of electrogenic secretion of chloride ions (Cl-) in mouse inner medullary collecting duct (mIMCD). The results show that adenosine does not regulate basal mIMCD electrogenic Cl- secretion. However, adenosine release during arginine vasopressin-stimulated electrogenic Cl- secretion binds to adenosine A1 receptors, thereby attenuating electrogenic Cl- secretion by reducing intracellular levels of cyclic adenosine monophosphate.

Swim training changes the effects of hemorrhage on endocrine and sympathoadrenal function in borderline hypertensive rats (BHR). In exercised-trained BHR rats, glucose mobilization is lower due to fluid and electrolyte conservation, possibly to conserve stores in response to hemorrhage. The altered sympathoadrenal and endocrine function can help ease the deleterious effects of hemorrhage.

The reverse transcriptase-polymerase chain reaction (PCR) and whole cell patch-clamp techniques confirm the presence of A1 adenosine receptors in normal and cystic fibrosis (CF) human airway epithelial cells and their ability to moderate Cl- transport in the cells. The sequence of the human brain adenosine A1 receptor are similar in the normal and CF airway cell PCR products. In normal epithelial cells, the adenosine 3',5'-cyclic monophosphate-activated Cl- conductance is enhanced by 8-cyclopentyl-1,3- dipropylxanthine.

MCCoy, David E., Amanda L. Taylor, Brian A. Kudlow, Katherine Karlson, Margaret J. Slattery, Lisa M. Schwiebert, Erik M. Schwiebert, and Bruce A. Stanton. Nucleotides regulate NaCl transport in mIMCD-K2 cells via P2X and P2Y purinergic receptors. Am. J. Physiol. 277 (Renal Physiol. 46): F552-F559, 1999.--Extracellular nucleotides regulate NaCl transport in some epithelia. However, the effects of nucleotide agonists on NaCl transport in the renal inner medullary collecting duct (IMCD) are not known. The objective of this study was to determine whether ATP and related nucleotides regulate NaCl transport across mouse IMCD cell line (mIMCD-K2) epithelial monolayers and, if so, via what purinergic receptor subtypes. ATP and UTP inhibited [Na.sup.+] absorption [measured via [Na.sup.+] short-circuit current ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII])] and stimulated [Cl.sup.-] secretion [measured via [Cl.sup.-] short-circuit current ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII])]. Using selective P2 agonists, we report that P2X and P2Y purinoceptors regulate [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] and [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]. By RT-PCR, two P2X receptor channels ([P2X.sub.3], [P2X.sub.4]) and two P2Y G protein-coupled receptors ([P2Y.sub.1], [P2Y.sub.2]) were identified. Functional localization of P2 purinoceptors suggest that [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] is stimulated by apical membrane-resident P2Y purinoceptors and P2X receptor channels, whereas [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] is inhibited by apical membrane-resident P2Y purinoceptors and P2X receptor channels. Together, we conclude that nucleotide agonists inhibit [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] across mIMCD-K2 monolayers through interactions with P2X and P2Y purinoceptors expressed on the apical plasma membrane, whereas extracellular nucleotides stimulate [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] through interactions with P2X and P2Y purinoceptors expressed on the apical plasma membrane. inner medullary collecting duct; short-circuit current; kidney

Determines whether adenosine and adenosine A1 receptors regulate electrogenic Cl- secretion in mIMCD-K2 cells. Cell culture; Measurement of short-circuit current; Permeable supports; Cell model depicting autocrine negative-feedback loop.

Presents a study regarding identification and function of A1 adenosine receptors in normal and cystic fibrosis human airway epithelial cells. Performance of RT-PCR on poly(A)+ RNA isolated from normal and CF airway epithelial cells; Use of Northern blot analysis to determine presence of poly(A)+ RNA transcripts encoding the A1 receptor.