[Isolated splenomegaly].
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Diagnosis, Differential↗
Biomedical subjects
C Wanning
Publications and source records attributed to C Wanning.
Cellular mechanisms of action of a ouabain-like factor in vascular smooth-muscle cells.
Ouabain-like factor (OLF) has been implicated to play an important role in certain forms of hypertension. We isolated OLF from the urine of salt-loaded healthy subjects by stepwise chromatographic procedures. The post-salt fraction (F IV) eluted from Sephadex G-25 was rechromatographed on Sephadex G-10. A late small-molecular-weight fraction F8 inhibited Na-K-ATPase in vitro (OLF activity). The effects of OLF on intracellular Ca2+ concentrations ([Ca2+]i) and pH (pHi) were examined in cultures of vascular smooth-muscle cells using the fluorescent probes fura-2 and 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF), respectively. Preincubation with OLF increased basal [Ca2+]i from 87 +/- 6 to 160 +/- 8 nM (p < 0.001) and enhanced arginine vasopressin-stimulated maximal [Ca2+]i (418 +/- 11 vs. 523 +/- 14 nM, p < 0.01). This effect was similar to that of ouabain. OLF also induced a rapid transient increase of [Ca2+]i (82 +/- 9 vs. 253 +/- 23 nM, p < 0.01); [Ca2+]i returned to levels slightly above baseline within approximately 4 min. OLF-stimulated [Ca2+]i was attenuated by verapamil (126 +/- 5 nM, p < 0.01) and was also reduced in Ca(2+)-free medium (104 +/- 9 nM, p < 0.01). As opposed to OLF, ouabain did not exhibit this fast transient effect on [Ca2+]i. Amiloride (10(-3) M) blocked the sustained effect of OLF on [Ca2+]i (77 +/- 11 vs. 86 +/- 12 nM, NS). OLF induced an increase of pHi from 7.09 +/- 0.03 to 7.28 +/- 0.04 (p < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effects of endothelin on sodium transport mechanisms: potential role in cellular Ca2+ mobilization.
The effects of endothelin on cellular Ca2+ mobilization were examined in cultured rat vascular smooth muscle cells (VSMC). Endothelin (10(-8)M) induced a rapid transient increase of [Ca2+]i from 77 +/- 3 to 104 +/- 5 nM (p less than .05) in VSMC. Preincubation (60 min) with endothelin (2 x 10(-6)M) increased basal [Ca2+]i from 77 +/- 3 to 105 +/- 8 nM (p less than .05). Preincubation with endothelin also enhanced vasopressin (10(-7)M)-stimulated peak levels of [Ca2+]i (528 +/- 20 nM vs 969 +/- 21 nM, p less than .01). Endothelin (10(-7)M) induced an intracellular alkalinization (7.18 +/- 0.03 vs 7.37 +/- 0.04, p less than .01) which was blocked by pretreatment with amiloride. The biphasic effects of endothelin on [Ca2+]i were similar to those of an endogenous inhibitor of Na-K-ATPase that we examined in a previous study. Therefore, we examined the effects of endothelin on Na-K-ATPase in an enzyme preparation from hog cerebral cortex. At high concentrations, endothelin (10(-5)M) inhibited Na-K-ATPase in vitro. Thus, endothelin may exert its vasoconstrictor effects at least in part via alterations of cellular Ca2+ mobilization in VSMC. While the rapid transient increase of [Ca2+]i appears to reflect intracellular Ca2+ mobilization, the sustained effect on [Ca2+]i may be related to an increase of intracellular sodium mediated by inhibition of Na-K-ATPase and/or more likely by stimulation of the Na+/H+-antiport.
Animals↗