scholarly journals Transmural calcium fluxes and role of mucins as cellular calcium-transport vehicles in chicken trachea in vitro.

1987 ◽  
Vol 388 (1) ◽  
pp. 121-140
Author(s):  
P W Kent ◽  
N Mian
1980 ◽  
Vol 238 (5) ◽  
pp. G424-G428
Author(s):  
H. Schiffl ◽  
U. Binswanger

Calcium ATPase, an enzyme involved in intestinal calcium transport, was measured in homogenates of duodenal mucosal scrapings of normal and uremic rats. The effects of calcium deprivation and treatment with 1 alpha,25-dihydroxycholecalciferol [1,25-(OH)2D3] were investigated as well. Uremia decreased the enzyme activity and impaired the rise after calcium deprivation as observed in intact rats. The 1,25-(OH)2D3 treatment increased the enzyme activity in uremic animals and resulted in an identical response to calcium deprivation as observed in intact rats; parathyroidectomy abolished this effect. A striking correlation between everted duodenal gut sac calcium transport and calcium ATPase activity could be demonstrated for all groups of rats studied. It is concluded that the calcium ATPase activity is linked to the production of 1,25-(OH)2D3 as well as to an additional factor, probably parathyroid hormone. The close relationship between enzyme activity and in vitro calcium transport, even during constant physiological supplementation with 1,25-(OH)2D3, suggests an autonomous role of the calcium ATPase activity for mediation of calcium transport in the duodenum in addition to the well-known mechanisms related to vitamin D and its metabolites.


1981 ◽  
Vol 240 (4) ◽  
pp. H561-H570
Author(s):  
M. L. Bhattacharyya ◽  
M. Vassalle

The effects of strophanthidin on electrical and mechanical events in canine cardiac Purkinje fibers were studied in vitro in the absence and presence of tetrodotoxin (TTX), norepinephrine, and high calcium. In Tyrode solution, strophanthidin (1-3 X 10(-7) M), norepinephrine (3-5 X 10(-7) M), and high calcium 8.1 mM) increased the force of contraction, and TTX markedly reduced it. In the presence of TTX, strophanthidin had little or no inotropic effect, whereas that of norepinephrine and high calcium was less than in Tyrode solution. In the presence of TTX, strophanthidin increased force markedly if (and as long as) either norepinephrine or high calcium were also present. A higher dose of strophanthidin (10(-6) M) induced a markedly delayed increase in force in presence of TTX. The results suggest that, in the presence of TTX, in a low concentration strophanthidin has little effect on force, because cellular calcium is low; however, it becomes effective when the calcium is increased by norepinephrine or high calcium. In toxic doses, strophanthidin increases force even in the presence of TTX as the inhibition of the pump should increase intracellular sodium and therefore calcium.


1977 ◽  
Vol 232 (3) ◽  
pp. E336
Author(s):  
J T Pento ◽  
L C Waite ◽  
P J Tracy ◽  
A D Kenny

The role of parathyroid hormone (PTH) in the adaptive response in gut calcium transport to calcium deprivation has been studied in the rat using both the in vitro everted duodenal sac and the in situ ligated duodenal segment technique. Intact or parathyroidectomized (PTX) young rats were placed on a low calcium (0.01%) diet for 7-, 14-, or 21-day adaptation periods and compared with control rats maintained on a high calcium (1.5%) diet. Prior PTX (3 days before the start of the adaptation period) abolished the adaptive response (enhanced calcium transport) induced by calcium deprivation for a 7-day adaptation period, but did not abolish a response after a 21-day period. A 14-day adaptation period gave equivocal results. It is concluded that PTH appears to be necessary for short-term (7-day) adaptation, but not for long-term (21-day) adaptation to calcium deprivation. However, if accessory parathyroid tissue is present, the data could be interpreted differently: the essentiality of PTH for the adaptive response might be independent of the length of the adaptation period. The data also contribute to a possible resolution of the controversy concerning the involvement of PTH in the regulation of intestinal calcium transport in the rat.


1979 ◽  
Vol 236 (4) ◽  
pp. F357-F364 ◽  
Author(s):  
J. E. Bourdeau ◽  
M. B. Burg

Thick ascending limbs of Henle's loop were dissected from rabbit kidneys and perfused in vitro. Unidirectional transepithelial calcium fluxes from lumen-to-bath and bath-to-lumen were measured with 45Ca using different solutions that caused the transepithelial voltage to vary over a wide range. With lumen-positive voltages there was net calcium absorption from lumen to bath which varied directly with the voltage. With voltage near zero there was no measurable net flux. When the voltage was made negative, the direction of net calcium transport reversed (i.e., secretion from bath to lumen). The presence or absence of bicarbonate in the lumen did not affect the calcium fluxes. Calcium permeability, calculated from the dependence of net flux on voltage, was 7.7 x 10(-6) cm/s, which is approximately 25% of the sodium permeability previously determined in this segment. Analysis of the calcium flux ratios revealed interdependence of the bidirectional fluxes consistent with single-file diffusion but no evidence for active calcium transport. We conclude that there is an important component of passive net calcium transport driven by the voltage in this segment.


1965 ◽  
Vol 208 (2) ◽  
pp. 370-374 ◽  
Author(s):  
Harold E. Harrison ◽  
Helen C. Harrison

The role of the permeability of intestinal mucosa to calcium was determined in rats by comparison of calcium transport in vitro across the wall of everted intestinal loops from which the mucosal epithelium was removed and of loops with intact epithelium. Energy-dependent transport systems were inhibited by incubation at 5 C or by addition of N-ethyl maleimide to the medium. The experiments were designed to measure calcium transport along a concentration gradient between mucosal and serosal surfaces at varying concentrations of calcium in the mucosal solution. The results indicate that the intact intestinal mucosa presents a diffusion barrier to calcium and that this diffusion barrier is lessened by vitamin D treatment of the animal from which the intestine is obtained.


1985 ◽  
Vol 249 (1) ◽  
pp. C117-C123 ◽  
Author(s):  
C. S. Hyun ◽  
E. J. Cragoe ◽  
M. Field

The role of alpha 2-adrenergic receptors in the regulation of intestinal Ca2+ transport was studied in vitro in rabbit proximal colon and distal ileum. Unidirectional mucosal-to-serosal and serosal-to-mucosal fluxes (Jm----s and Js----m) of 45Ca2+ were measured across isolated mucosal sheets bathed on both sides with identical Ringer solutions (1.25 mM Ca2+) and short-circuited. In the proximal colon, mucosal-to-epithelial influx (Jm----e) of Ca2+ was also determined. Proximal colonic mucosa secreted Ca2+ (in nmol X h-1 X cm-2, Jm----s = 12.1 and Js----m = 42.2). Epinephrine (10 microM) abolished Ca2+ secretion (Jm----s = 24.1 and Js----m = 24.9) but did not affect Jm----e (21.4 in controls and 23.6 after epinephrine). These effects were mediated by alpha 2-adrenergic receptors: yohimbine abolished the effect of epinephrine, but prazosin and propranolol did not; furthermore, clonidine mimicked the effects of epinephrine, whereas methoxamine and isoproterenol had no effect. Ileal mucosa did not transport Ca2+ spontaneously; epinephrine (10 microM) increased Jm----s in the ileum without affecting Js----m, thereby stimulating net Ca2+ absorption. The mechanism for these alpha 2-receptor-mediated effects was examined in proximal colon. The effect of epinephrine on Jm----s was dependent on serosal Na+ but was unaffected by ouabain or the Na+-Ca2+ exchange inhibitor, benzamil. The effect of epinephrine on Js----m was dependent on serosal Na+ and was blocked by both ouabain and benzamil. In the absence of epinephrine benzamil did not alter Jm----s or Js----m.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 240 (6) ◽  
pp. G424-G431 ◽  
Author(s):  
H. N. Nellans ◽  
R. S. Goldsmith

Transepithelial calcium transport has been investigated in rat cecum under in vitro voltage-clamp conditions. Under short-circuit conditions, the cecum behaves as a relatively tight epithelium for calcium fluxes, where mucosal-to-serosal (JCam leads to s) flux exceeds the reverse flux by at least 15-fold. JCanet is abolished in the presence of 1 mM N-ethylmaleimide, is inhibited by 40% with 1 mM ouabain, and is decreased by at least 60% when medium sodium is replaced by choline. Voltage-clamping experiments suggest that both electroneutral- and electrogenic-mediated calcium fluxes traverse the cell in the mucosal-to-serosal direction. Serosal-to-mucosal flux is purely diffusional and probably constrained to the paracellular pathway. In rats weighing less than 175 g, a low-calcium diet has no significant stimulatory effect on JCam leads to s, but a high-calcium diet markedly reduces this flux. These results suggest that the cecum possesses the highest density of calcium transport sites in the rat intestine and is ideally suited for bulk calcium absorption, which may be “down regulated” in response to an increased calcium load in growing animals.


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