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C Knoblauch

Publications and source records attributed to C Knoblauch.

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Regulatory volume decrease by cultured renal cells.

Volume regulatory responses of OK cells (a continuous epithelioid cell line from opossum kidney) are examined by electronic cell sizing and measurements of intracellular pH in cell suspensions. In response to a 40% reduction in osmolality, the cells swell and then subsequently shrink toward their starting volume. This regulatory volume decrease (RVD) is reduced by replacement of Cl- in the medium with acetate. Replacement of Cl- with NO3- accelerates the RVD. The RVD response is inhibited by 1 mM quinine or 100 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in the medium. The inhibitory effect of 100 microM DIDS (but not 1 mM quinine) is altered by replacement of Cl- by NO3- in the medium. Hypotonic challenge does not induce a DIDS-sensitive net flux of acid-base equivalents. Addition of (9 microM) valinomycin also inhibits the RVD response. It is suggested that the RVD response of OK cells involves activation of separate K+ and Cl- channels.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid

Separate control of regulatory volume increase and Na+-H+ exchange by cultured renal cells.

Suspensions of OK cells (a continuous epithelioid cell line from opossum kidney) are examined by electronic cell sizing, measurements of intracellular pH, and measurements of cellular Na+ and K+. The response of the cells to hypertonic solutions is evaluated in most detail. When shrunken by exposure to hyperosmotic medium (430 mosmol/kg), the cells do not demonstrate a regulatory volume increase (RVI) independent of the solute that is used to increase osmolality [NaCl, N-methyl-D-glucamine-HCl (NMGCl), or sucrose]. In contrast, when cells are preexposed to 190 mosmol/kg medium and then shrunken by exposure to 310 mosmol/kg medium, a volume increase is observed after the addition of 120 mosmol/kg NaCl or NMGCl, but not sucrose. This RVI is sensitive to 1 mM furosemide and removal of Na+ or K+ from the medium, but it is not inhibited by 1 mM amiloride. In the presence of a propionate-induced cellular acidification, a Na+-H+ exchanger in the cells is shown to have a large capacity for net solute uptake and to be inhibited by 1 mM amiloride. Net solute uptake by the Na+-H+ exchanger is sensitive to addition of parathyroid hormone or 8-bromoadenosine 3',5'-cyclic monophosphate but is not stimulated in response to cell shrinkage.

8-Bromo Cyclic Adenosine Monophosphate