Renin expression in the kidney and brain is reciprocally controlled by captopril

The tissue distribution of rat renin mRNA was examined. Sensitive RNase protection analyses demonstrated that renin mRNA are produced by the extra-renal tissues such as adrenal, brain, liver, lung, pituitary and testis. In response to sodium depletion and captopril treatment, the expression of mRNAs encoding rat renin were in a tissue-specific manner. The level of kidney renin mRNA remarkably increased in sodium-depleted rats treated with captopril, whereas that of brain renin mRNA definitely decreased. No significant change in the level of liver renin mRNA was observed after the same treatment. These results suggest that the expression of cerebral renin is regulated by physiological stimuli independent of its extra-cerebral expression.     

Para-aminohippuric acid secretion by the vertebrate kidney

Tubular secretory capacity has been investigated in the kidney of marine fishes Scorpaena porcus, Spicara smaris, frog Rana ridibunda and albino rat by determination of maximal transport of p-aminohippurate--TmPAH, Following values of Tmax expressed in mg/hour per 100 g of body weight were obtained: 0.73 +/- 0.17 for S. porcus, 0.92 +/- 0.09 for S. smaris, 0.93 +/- 0.10 for R. ridibunda and 15.6 +/- 1.6 for rats.     

Electrogenic bicarbonate secretion by prairie dog gallbladder

Pathological rates of gallbladder salt and water transport may promote the formation of cholesterol gallstones. Because prairie dogs are widely used as a model of this event, we characterized gallbladder ion transport in animals fed control chow by using electrophysiology, ion substitution, pharmacology, isotopic fluxes, impedance analysis, and molecular biology. In contrast to the electroneutral properties of rabbit and Necturus gallbladders, prairie dog gallbladders generated significant short-circuit current (I(sc); 171 +/- 21 microA/cm(2)) and lumen-negative potential difference (-10.1 +/- 1.2 mV) under basal conditions. Unidirectional radioisotopic fluxes demonstrated electroneutral NaCl absorption, whereas the residual net ion flux corresponded to I(sc). In response to 2 microM forskolin, I(sc) exceeded 270 microA/cm(2), and impedance estimates of the apical membrane resistance decreased from 200 Omega.cm(2) to 13 Omega.cm(2). The forskolin-induced I(sc) was dependent on extracellular HCO(3)(-) and was blocked by serosal 4,4'-dinitrostilben-2,2'-disulfonic acid (DNDS) and acetazolamide, whereas serosal bumetanide and Cl(-) ion substitution had little effect. Serosal trans-6-cyano-4-(N-ethylsulfonyl-N-methylamino)-3-hydroxy-2,2-dimethyl-chroman and Ba(2+) reduced I(sc), consistent with the inhibition of cAMP-dependent K(+) channels. Immunoprecipitation and confocal microscopy localized cystic fibrosis transmembrane conductance regulator protein (CFTR) to the apical membrane and subapical vesicles. Consistent with serosal DNDS sensitivity, pancreatic sodium-bicarbonate cotransporter protein pNBC1 expression was localized to the basolateral membrane. We conclude that prairie dog gallbladders secrete bicarbonate through cAMP-dependent apical CFTR anion channels. Basolateral HCO(3)(-) entry is mediated by DNDS-sensitive pNBC1, and the driving force for apical anion secretion is provided by K(+) channel activation.     

Gonadotroph-rich cell lines derived from pituitary clonal cells (2A8) grafted under the kidney capsule

Summary Gonadotroph-rich cell lines were established from multipotential pituitary clonal cells (2A8) which were implanted under kidney capsule of hypophysectomized female rats. These cell lines secrete gonadotrophins (FSH and LH) continuously over two months after establishment; LHRH stimulated the secretion of hormones into the culture medium. Many of the cells reacted immunohistochemically to antiserum to FSH or LH, while a small number reacted to antiserum to prolactin or TSH. They did not contain normal secretory granules such as those of gonadotrophs in vivo.Supported by USPHS Grant HD 11826 and NIH Grant P30 HD 10202. The authors wish to thank James Chambers (Immunocytochemistry), and Pat Koym and John Rhode (Radioimmunoassay) for their excellent technical assistance. We also express our thanks to NIAMDD for providing pituitary hormones     

Inhibition of chymase reduces vascular proliferation in dog grafted veins

In this study, new methods are used to control cellular membrane tension to evaluate the role it plays in electrofusion. The data show that membrane tension present during the application of an electric field facilitates electro-induced membrane fusion. No enhancement was detected if the strain was applied after the pulse. Analysis of the electromechanical process of fusion revealed a synergy between the two kinds of constraints in the membrane fusion. Both mechanical and electrical constraints apparently play a key role in membrane fusion between the granule membrane and the plasma membrane, i.e. the exocytosis process.     

Quantitative anatomy of the dog kidney

Certain quantitative data on stereological indices reflecting the canine kidney tissue element parameters are presented.     

Uptake of 22Na+ by cultured dog kidney cells (MDCK).

22Na+ uptake measurements were conducted on the dog kidney cell line, MDCK, to determine the mechanism of ouabain-insensitive sodium transport. The radioisotope was found to be taken up into monolayer cultures via an ATP-independent, saturable process (Km = 40 mM). The presence of sodium on the opposite side of the membrane gave rise to a transstimulation of the 22Na+ flux. Studies utilizing potassium and valinomycin suggested that the transport system was insensitive to changes in the membrane potential. Replacement of chloride in the assay buffer with other anions did not decrease the rate of 22Na+ uptake at 14 mMNa+, but bicarbonate and acetate were stimulatory. Potassium and rubidium increased the rate of 22Na+ influx (Ka = 13mM with 14 mM NaCL in the medium). Lithium (Ki = 7.5mM) and amiloride (Ki = 1.7 x 10(-5) M) were competitive and partially (or mixed) competitive inhibitors, respectively. The data are consistent with a mechanism of sodium uptake that includes a carrier(s) capable of catalyzing net sodium uptake and sodium-sodium exchange.