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J Goyal

Publications and source records attributed to J Goyal.

14 recordsLinked to original sources
PubMed1991

Cell density modulates the decrease of cytosolic free Ca2+ induced by atrial natriuretic hormone, S-nitroso-N-acetylpenicillamine and 8-bromo cyclic GMP in cultured rat mesangial cells.

Cyclic GMP-elevating agents, including atrial natriuretic hormone and NO-generating vasodilators, decrease cytosolic free Ca2+ levels in mesangial cells. We have investigated the role of cell density as a modulator of the decrease in cytosolic free Ca2+ induced by the cyclic GMP (cGMP)-elevating vasodilators atrial natriuretic peptide (99-126) [ANP (99-126); 'atriopeptin 28'] and the NO-generating vasodilator S-nitroso-N-acetylpenicillamine (SNAP), in cultured rat mesangial cells. Increasing cell density was significantly correlated with the decrease in cytosolic free Ca2+ induced by ANP (99-126) or SNAP. Moreover, this effect was independent of the cells' proliferative status. ANP (99-126) and SNAP induced greater fold stimulation of cGMP accumulation in high-density cells, but the levels of cGMP elicited by high concentrations of ANP (99-126) or SNAP were similar in high- and low-density cells. 8-Bromo cGMP was more effective in decreasing cytosolic free Ca2+ in high- than in low-density cells, suggesting that the greater effectiveness of ANP (99-126) and SNAP was, in part, due to greater effectiveness of endogenous cGMP in high-density cells. The results document that cell density, but not proliferative status, plays an important role in the modulation of intracellular Ca2+ dynamics in rat mesangial cells by atriopeptins, NO-generating vasodilators and cGMP.

Animals↗
PubMed1991

Role of calcium and calmodulin in Giardia lamblia-induced diarrhoea in mice.

The unidirectional fluxes of Na+, Cl- and Ca2+ across the small intestinal epithelium of normal and Giardia lamblia-infected mice were studied in vitro in short-circuited tissue. Net secretion of Na+ and Cl- was observed in infected animals, whereas in non-infected (control) animals there was net absorption of Na+ ions and marginal secretion of Cl- ions. In infected animals, net absorption of Ca2+ was observed as compared to little secretion observed in control animals. Although the presence of Ca(2+)-ionophore in the medium resulted in a net secretion of Na+ and Cl- in controls, it could not cause any change in the fluxes of these ions in infected animals. Verapamil, a calcium channel blocker, reversed the effects of infection and Ca(2+)-ionophore. Further W7 (n-(6-aminohexyl)-5 chloro-1-naphthalene sulphonamide), a calmodulin antagonist, also reversed the effects of infection. The addition of the neurotoxin, tetrodotoxin caused net absorption of Na+, Cl- and net secretion of Ca2+ in the control group, but it could not produce any effect on the fluxes of these ions in the infected group. These findings demonstrate that, in G. lamblia infection, the secretion of Na+ and Cl- is associated with an increase in absorption of Ca2+ and an increase in calmodulin activity in intestinal microvillar core. These findings further suggest that the enteric nervous system plays a marginal role in Giardia infection.

Animals↗
PubMed1990

Differences between the mechanisms of action of heat-stable and heat-labile enterotoxins of Escherichia coli.

The mucosal-to-serosal and serosal-to-mucosal fluxes of Na+ and Cl- were measured in control mice and mice treated with heat-stable (ST) and heat-labile (LT) enterotoxins in the presence or absence of: Ca2(+)-ionophore A23187, an activator of Ca2(+)-calmodulin; or phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C(PKC); or 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine (H-7), an inhibitor of PKC. There was net secretion of Na+ and CL- in both experimental groups in contrast to net absorption in the control group. The addition of ionophore or PMA or ionophore + PMA resulted in net secretion of Na+ and Cl- in the control group and the effect of ionophore and pMA was found to be additive. The addition of ionophore did not cause any change in electrolyte fluxes in the ST toxin treated group, however, it increased the net secretion of Na+ and Cl- in the LT toxin treated group. PMA increased the net secretion of Na+ and Cl- in the St toxin treated group, however, it did not cause any change in Na+ and Cl- fluxes in the LT toxin treated group. H-7 did not reverse the effect of ST toxin, however, it reversed the effect of LT toxin.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Calcium calmodulin in altered NaCl transport by heat-labile enterotoxin of Escherichia coli.

The mucosal-to-serosal and serosal-to-mucosal fluxes of Na+ and Cl- were carried out in control and experimental groups treated with different doses of heat-labile enterotoxin in the presence or absence of Ca2+-ionophore, Ca2+ channel blocker and calmodulin inhibitor. There was net secretion of Na+ and Cl- in 16 and 32 units of heat-labile enterotoxin treated groups in comparison to net absorption in control group, however, in animals treated with 8 units of heat-labile enterotoxin, no change in Na+ and Cl- fluxes was found when compared to control. Ca2+- ionophore increased net secretion of Na+ and Cl- in 16 and 32 units of heat-labile enterotoxin treated groups and also caused secretion in control group instead of net absorption. Ca2+ channel blocker and calmodulin inhibitor partially reversed the effect of heat-labile enterotoxin. The effect of Ca2+-ionophore was more pronounced in the control group while that of Ca2+ channel blocker and calmodulin inhibitor was more pronounced in 16 and 32 units of heat-labile enterotoxin treated groups. The findings suggest the involvement of Ca2+ and calmodulin in the action of heat-labile enterotoxin of Escherichia coli in mice.

Animals↗
PubMed1989

Effect of heat-stable and heat-labile enterotoxins of Escherichia coli on intestinal brush border membrane enzymes of mice.

The activities of intestinal brush border membrane (BBM) enzymes alkaline phosphatase, maltase, lactase, sucrase, gamma-glutamyl transpeptidase and leucine aminopeptidase were determined in intestinal homogenates and purified BBMs from control, heat-stable and heat-labile enterotoxin treated mice. The activities of all the enzymes except lactase were decreased significantly (p less than 0.01) in homogenates while increased significantly (p less than 0.001) in BBMs of experimental groups as compared to controls. Calmodulin activities were increased significantly (p less than 0.01) as compared to control in heat-stable enterotoxin treated mice but remained unaltered in heat-labile enterotoxin treated mice. DNA contents of intestinal homogenates were decreased in experimental groups demonstrating the decrease in cell number in these groups. The altered BBM enzyme activities could not be attributed to changes in calmodulin activities. The increase in enzyme activities in BBMs may reflect a compensatory phenomenon in the remaining cells.

Alkaline Phosphatase↗
PubMed1989

Role of Ca2(+)-calmodulin and protein kinase C in the secretory action of heat-labile enterotoxin of Escherichia coli in mice.

The mucosal-to-serosal and serosal-to-mucosal fluxes of Na+ and Cl- were carried out in control and heat-labile enterotoxin treated mice in the presence or absence of Ca2(+)-ionophore A23187, the activator of Ca2(+)-calmodulin or Phorbol-12-myristate-13-acetate (PMA), the activator of Protein kinase C (PKC) or 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine (H-7), an inhibitor of PKC. There was net secretion of Na+ and Cl- in experimental group in comparison to net absorption in control group. The addition of ionophore or PMA resulted in net secretion of Na+ and Cl- in control group. In experimental group ionophore increased the net secretion of Na+ and Cl- while, PMA could not cause any change in Na+ and Cl- fluxes in experimental group. Calmodulin activity remained unaltered in heat-labile enterotoxin treated mice as compared to control. H-7, reversed the effects of PMA and heat-labile enterotoxin. These studies demonstrate that heat-labile enterotoxin primarily involves PKC in its action.

Animals↗
PubMed1988

Physiological and histopathological changes in the intestines of mice challenged with S. typhi.

Transport of Na+, Cl-, Ca2+ and 3-0-methyl-D-glucose (a non-metabolizable analogue of D-glucose) was worked out in control, infected and immunized-infected animals along with histopathological studies of the intestines in these groups. There was significant decrease (p less than 0.01) in net absorption of Na+ and Cl- in the infected group as compared to that in the control group. There was also a significant decrease (p less than 0.01) in 3-0-methyl-D-glucose uptake in the infected group. However, no change was found in the immunized group in any of the electrolytes and non-metabolizable analogue of D-glucose. These findings correlated well with the histopathological studies as the infected intestines showed complete disorganization of mucosal tissues with loss of epithelial cells from the villi whereas the mucosal lining and epithelial cells from the intestines of immunized mice were normal looking.

3-O-Methylglucose↗
PubMed1988

Effect of excretory-secretory products of Giardia lamblia on glucose and phenylalanine transport in the small intestine of Swiss albino mice.

The transport of D-glucose and L-phenylalanine was measured in intestinal brush border membrane (BBM) vesicles treated with Excretory-secretory (ES) products of Giardia lamblia. Uptake was found to be significantly lower (P/0.01) in the treated vesicles than in the controls. Exposure of intestinal tissue to ES products resulted in net secretion (P/0.01) of Na+, C1- and 3-O-methyl-D-glucose. Both observations indicate that alterations in the absorptive functions of the intestine might be attributed to interaction of ES products with the BBM.

Animals↗
PubMed1987

Studies on the mechanism of Escherichia coli heat-stable enterotoxin-induced diarrhoea in mice.

The unidirectional fluxes of Na+, Cl- and Ca2+ and activities of calmodulin in the intestinal microvillar core were studied in Escherichia coli heat-stable enterotoxin-treated mice. There was net secretion of Na+ and Cl- in toxin-treated animals, while in control animals there was net absorption of these ions. In both control and experimental animals, there was net absorption of Ca2+; however, the absorption was significantly higher (P less than 0.01) in experimental animals when compared to controls. In the presence of Ca2+-ionophore, there was a net secretion of Na+ and Cl- in controls, while the Ca2+-ionophore could not cause any change in the fluxes of these ions in experimental animals. The activity of calmodulin was significantly higher (P less than 0.01) in experimental animals. Verapamil, a calcium channel blocker, and trifluoperazine, a calmodulin inhibitor, reversed the effects of Ca2+-ionophore and heat-stable enterotoxin. These studies demonstrate that the toxin acts through Ca2+-calmodulin, and secretion of Na+ and Cl- in experimental animals is due to an increase in calcium absorption and an increase in calmodulin activity in the intestinal microvillar core.

Animals↗
PubMed1987

Role of Ca2+/calmodulin in the regulation of sugar uptake in Escherichia coli heat-stable enterotoxin induced diarrhoea in mice.

The mucosal-to-serosal fluxes of 3-O-methyl-D-glucose, a non-metabolizable analogue of D-glucose, were carried out in control and heat-stable enterotoxin treated mice in the presence or absence of Ca2+-ionophore, Ca2+-channel blocker, calmodulin inhibitor and Na+-K+-ATPase inhibitor. The transport of the sugar was significantly decreased (p less than 0.01) in the experimental animals. In the presence of Ca2+-ionophore, the uptake of the sugar decreased significantly (p less than 0.01) only in the control group while experimental group remained unaffected. Ca2+ channel blocker and calmodulin inhibitor significantly increased (p less than 0.01) the uptake of sugar in both the groups, however, the changes were more pronounced in the experimental group. Ouabain blocked the uptake of the sugar in both the groups. These studies indicated that heat-stable enterotoxin inhibit Na+-K+-ATPase by increasing Ca2+ uptake and calmodulin activity, thus resulting in decreased uptake of 3-O-methyl-D-glucose in heat-stable enterotoxin treated mice.

3-O-Methylglucose↗
PubMed1976

Spinal retroflexion in craniorhachischisis: its classification and limitations.

Spinal retroflexion has been studied in five stillborn human fetuses having craniorhachischisis. The findings show that retroflexion in this variant of anencephaly can be classified into severe, moderate and mild forms. The three grades can be differentiated from one another by the direction of the face, shape of the mentothoracic junction, extension of hairline on back, radiographic abnormalities of the spine, and the diaphragmatic defects. It is discussed that, though the anencephalies with severe or moderate degree of cervical retroflexion resemble iniencephaly in their features of spinal retroflexion, those having mild retroflexion are contrasted and should not be categorised with iniencephaly. It is suggested that for precision the term "spinal retroflexion" should be used after duly prefixing it by an appropriate word (severe, moderate or mild) indicating the degree of retroflexion observed.

Abnormalities, Multiple↗