Adenosine triphosphate--dependent calcium uptake by rat submaxillary gland microsomes.

Microsomes from rat submaxillary glands are able to take up calcium from the suspension media. Calcium uptake is greatly increased by the presence of ATP. This effect of ATP is not detected at 0 degrees C. ADP cannot replace ATP to potentiate calcium uptake. ATP-dependent calcium uptake is not observed in the absence of magnesium. ATP-dependent calcium uptake is enhanced by oxalate and, to a lesser degree, by inorganic phosphate. Total calcium per milligram of microsomal protein observed when tests were performed without oxalate closely parallels the amounts for skeletal and cardiac muscles reported by several authors. Calcium uptake in salivary gland microsomes is slower than in muscle microsomes. Speculations are considered about the role of ATP-dependent calcium uptake. It is suggested that a decrease in intracellular free calcium levels returns these cells to the resting state after secretion.

Comparative effect of antiinflammatory drugs on rat paw edema induced by human sterile dental plaque extract, carrageenan or dextran.

The effect of antihistamine (diphenhydramine) or antihistamine and antiserotonin (cyproheptadine) or aspirin-like (acetylsalicylic acid and indomethacin) or corticosteroid (dexamethasone) drugs on the edema induced by various doses of carrageenan, dextran or human sterile dental plaque extract, injected intraplantarily in the rat paw were comparatively studied. The results showed that: (a) human dental plaque extract injected into the rat paw induces a dose-dependent inflammatory response, confirming that it is a potent phlogistic agent; (b) the edema induced by the plaque extract though closer to the pattern of carrageenan-induced edema, was different to both the carrageenan- and the dextran-induced edema in its time course and the response to antiedema drugs; (c) histamine and serotonin are liberated in the plaque-induced edema but they play no essential role; (d) the inhibitors of arachidonic acid metabolite formation (ASA, indomethacin and dexamethasone) inhibit this inflammation suggesting the presence of prostaglandin-like substances since its first phase.

Effect of a toothpaste containing amyloglucosidase and glucose oxidase on recurrent aphthous ulcers.

The aim of this study was to assess whether a toothpaste containing amyloglucosidase and glucose oxidase (Z) provoked any effect on minor recurrent aphthous ulcers, (RAU) as compared with a placebo toothpaste (P). Twenty patients (11 females), suffering from minor RAU, participated in this study during a period of 15 weeks. The patients brushed their teeth twice a day with the toothpaste. They were examined once a week to monitor the number and size of ulcers. The mean number of ulcers in both groups was about 40% lower than that found before treatment. Ulcer mean diameter had also decreased in both the placebo (about 32%) and experimental groups (about 66%). There were no statistically significant differences between the two groups in number of weeks with ulcers, in total number of ulcers per patient, and in mean diameter of the ulcers. In conclusion, no significant differences in therapeutic effects could be shown between treatments with Z and P.

Reserpine non-selectively inhibits rat uterus contraction in vitro.

1. Reserpine produced a direct in vitro non-selective inhibitory effect on smooth muscle contraction of endometrium-free rat uterus. 2. Reserpine uptake into uterine muscle and its antagonistic effect on contraction had a similar time course. 3. Reserpine had a relaxing effect similar to that of trifluoperazine and different from that of verapamil or papaverine, and also failed to exert any inhibitory effect on 45Ca uptake rate. 4. Both reserpine and trifluoperazine but not verapamil inhibited the acetylcholine-induced contraction when present during the Ca-release from intracellular stores. 5. It is hypothesized that reserpine exerts its inhibitory action intracellularly on the activation of smooth muscle contraction by sarcoplasmic Ca2+.

Effects of ovarian hormone treatment on Ca(2+)-induced contractions and Ca(2+)-antagonism in the depolarized rat myometrium.

The effects of estrogen (E), progesterone (P) and estrogen plus progesterone (E+P) treatment on Ca-induced contraction in the KCL-depolarized uterine muscle, and the influences on the Ca2+ antagonism induced by reserpine and verapamil "in vitro" were studied. Uterine muscles from rats in estrus were taken as controls. Uteri from spayed untreated rats showed the same sensitivity to Ca2+ as those from estrus rats, but castration decreased maximal contractile tension to Ca2+ and Ca2+ threshold. P treatment failed to modified the effects of castration on the responses to Ca2+. E or E+P treatments decreased the sensitivity to Ca2+ but only E+P increased slope values and maximal contractile tension. E and E+P increased the potency of verapamil Ca2+ antagonism but none of the treatments modified reserpine direct inhibitory effects. The results obtained suggest that alterations on uterine contractility by hormone treatment are the result of complex interactions between both genomic effects on the contractile process as well as non-genomic direct actions of the hormones on Ca2+ membrane permeability.

Effects of calcium and EDTA on rat skin capillary permeability and on its response to histamine, serotonin and bradykinin.

Evans blue extravasation in rat skin was used to study the effects of Ca2+ and EDTA on vascular permeability and on its response to mediators of inflammation. Ca2+ induced a concentration-dependent decrease of vascular permeability. The opposite effect was seen with EDTA 0.2 mM or higher. Effects on vascular permeability of intradermically injected histamine 100 micrograms/ml, serotonin 5 micrograms/ml and bradykinin 5 micrograms/ml, were lower when Ca2+ 8 mM was injected in the same site, and higher when EDTA 2 mM was given. EDTA effects were inhibited by Ca2+. The results suggest that, in rat skin, Ca2+ decreases capillary permeability and its response to histamine, serotonin and bradykinin.

Specific opiate effects on dextran-induced inflammation in rats.

The effects of opiates were investigated in two models of acute inflammation in rats. Morphine (0.1-10 mg/kg, i.p.) inhibited by 50% the paw edema induced by interdigital injection of 1% dextran solution. Low but not high doses of naltrexone produced a similar degree of inhibition. Naltrexone (10 mg/kg, i.p.) completely prevented morphine antiedema effect. Local anesthesia of the hindleg with lidocaine neither modified dextran-induced paw edema nor morphine inhibitory effects. Morphine (10 mg/kg, i.p.) enhanced by 50% skin vascular permeability induced by intradermically injected 1% dextran solution. Again, naltrexone prevented morphine effects. The obtained results suggest a specific modulatory role of opiates in the acute inflammatory responses of the rat.

Effects of calcium and its antagonists on histamine-induced leakage in rat skin.

Evans blue extravasation in rat skin was used to study the effects of calcium, lanthanum, L-type calcium channel blockers and trifluoperazine on histamine-induced leakage. Histamine effect was inhibited by calcium 1-2.5 mM, lanthanum 1-10 mM, nifedipine 0.1 and 1 microM and trifluoperazine 30 and 100 microM. The effects of calcium decreased progressively as its concentrations rose up to 10 mM. The association of nifedipine 0,1 microM or trifluoperazine 30 microM with calcium 3 microM increased the inhibitory effects. Calcium 10mM reversed the effect of nifedipine 0.1 microM but not that of lanthanum 1 mM or trifluoperazine 30 microM. It is proposed that the effect of calcium on histamine-induced leakage is the expression of a balance between an extracellular inhibitory effect and an intracellular enhancing effect.