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Examines the role of epithelial transport in the cause of polycystic kidney disease. Characteristics of epithelial cells; Information on cystic ductal cells; Details on the genetics involved with autosomal polycystic kidney disease; Identification of the transport mechanisms involved in th cause of cystic fibrosis.

Presents a study which determined the intrinsic capacities of inner medullary collecting ducts (IMCD) in absorbing the secreting solutes and fluid in an isotonic medium using an in vitro method in rat kidneys. Discussion on renal sodium chloride excretion; Methodology; Effects of serum proteins on fluid secretion; Studies to evaluate cellular mechanisms of solute and fluid secretion in IMCD.

Investigates the occurrence of autocrine extracellular purinergic signaling in epithelial cells from polycystic kidneys (PK). Genetic forms of PK disease; Production of adenosine triphosphate (ATP) in epithelial monolayers; Mechanisms contributing to enhanced ATP release.

cAMP stimulates the in vitro proliferation of renal cyst epithelial cells by activating the extracellular signal-regulated kinase pathway. Background. Cellular proliferation is a key factor in the enlargement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD). We determined the extent to which adenosine 3′:5′-cyclic monophosphate (cAMP) may regulate the in vitro proliferation of cyst epithelial cells derived from human ADPKD cysts. Methods. Epithelial cells from cysts of individuals with ADPKD and from normal human kidney cortex (HKC) of individuals without ADPKD were cultured. The effects of agonists and inhibitors on the rate of cellular proliferation and the activation of extracellular signal-regulated kinase (ERK1/2) were determined. Results. 8-Br-cAMP (100 μmol/L) stimulated the proliferation of cells from eight different ADPKD subjects to 99.0% above baseline; proliferation was inhibited by protein kinase A (PKA) antagonists H-89 (97%) and Rp-cAMP (90%). Forskolin (10 μmol/L), which activates adenylyl cyclase, increased proliferation 124%, and receptor-mediated agonists arginine vasopressin, desmopressin, secretin, vasoactive intestinal polypeptide, and prostaglandin E2 stimulated proliferation 54.2, 56.3, 46.7, 37.1, and 48.3%, respectively. The mitogen extracellular kinase (MEK) inhibitor PD98059 completely inhibited ADPKD cell proliferation in response to cAMP agonists, but genistein, a receptor tyrosine kinase inhibitor, did not block cAMP-dependent proliferation. cAMP agonists increased the activity of ERK above control levels within five minutes. In contrast to ADPKD, proliferation and ERK activity of cells derived from normal HKC were not stimulated by cAMP agonists, although electrogenic Cl- secretion was increased by these agonists in both ADPKD and HKC cell monolayers. Conclusions. We conclude that cAMP agonists stimulate the proliferation of ADPKD but not HKC... [ABSTRACT FROM AUTHOR]