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PubMed1993

Distribution of anionic sites during increasing tight junctional permeability in the rat submandibular gland.

We sought to determine the effect of substance P salivary stimulation on both electrical charges and cellular permeability in the tight junctions of rat submandibular gland cells. Microperoxidase (1,900 daltons) was used as a tracer. It was administered by close-arterial infusion via the glandular arteries, and secretory routes of acinar cells in the gland were determined cytochemically. In the resting gland, microperoxidase reaction product filled the lateral intercellular spaces up to the tight junctions, but did not penetrate them. In the substance P-stimulated gland, microperoxidase reaction product was present within tight junctions and the lumen. Both distribution and mobility of anionic sites on the surface of the submandibular gland cells were studied utilizing multivalent ligand, ruthenium red and cationized ferritin as probes. In the resting gland, ruthenium red deposits were located uniformly in all areas of the basal membrane and intercellular spaces except for the tight junctional region of acinar and ductal cells. In substance P-stimulated gland, ruthenium red deposits were present in the tight junctional region and, to a lesser extent, in the intercellular spaces. Electrical charges of the tight junctions area of the lateral plasma membrane were studied using intraductal injection of cationized ferritin. In the resting gland, cationized ferritin probe was present in the intercellular spaces and was bound weakly in the tight junctional region. In the substance P-stimulated gland, cationized ferritin was firmly adherent to the tight junctional region.

Animals↗
PubMed1987

[Roles of kidney and submandibular gland in the release of rat plasma inactive renin].

In this study we outlined the development of an enzymatic technique to activate plasma inactive renin by trypsin in rat plasma. Using this method, we reported the releasing mechanism of the trypsin-activable inactive renin which has not yet been clarified. Adult male Wistar rats (260-300 g) were kept on regular diet (Na: 260 mg/100g) unless explained and underwent operation under pentobarbital anesthesia (50 mg/kg). Blood samples were obtained from conscious rats through the cannulae, which had been inserted into the left femoral arteries 24h before the experiments. After addition of excessive renin substrate which had been obtained from the 24 h-nephrectomized rat plasma, renin was measured by the commercial RIA-kit (Dainabot). Trypsin (Worthington) treatment (20 mg/ml plasma for 10 min at 4 degrees C) was followed by addition of SBTI (Sigma) (20 mg/ml plasma). This condition maximally increased the rate of angiotensin I generation and did not alter the Km or optimum pH of the renin reaction. In this condition, trypsin reaction was completely inhibited by adding these concentrations of SBTI. The molecular weight of inactive renin (51,000) in the normal rat plasma estimated by Sephadex G-100 column (Pharmacia) was the same as that in the nephrectomized rat plasma. In conclusion, trypsin treatment of plasma (20 mg/ml plasma for 10 min at 4 degrees C) followed by SBTI (20 mg/ml plasma) was justified for trypsin activation of rat plasma. Using this method, we investigated the changes in active and inactive renin after bilateral nephrectomy in the salt-depleted rat. Active renin decreased rapidly after bilateral nephrectomy with a half life of 23.6 +/- 4.0 min. Inactive renin, on the other hand, increased gradually and reached to a plateau 24 h after bilateral nephrectomy, and was kept unchanged during the following 24 h. The infusion of mouse submandibular gland active renin or angiotensin II could not prevent the increase of plasma inactive renin in the nephrectomized rat. These suggest that there may be no feedback mechanisms between plasma inactive and active renin or angiotensin II. Furthermore, we investigated the organ-related sources of plasma inactive renin which markedly increased after total nephrectomy. Simultaneous removals of submandibular glands but not of adrenal glands completely prevented the postnephrectomy increases of plasma inactive renin. But, removals of submandibular glands or adrenal glands alone were followed by no changes in the basal levels of plasma inactive renin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Tonin-like activity present in the human submandibular gland.

An enzyme which is able to liberate angiotensin II from angiotensin I, angiotensinogen(1-14) fragment and angiotensinogen was purified from human submandibular gland. Its molecular weight is 110,000; is inhibited by PMSF but not by EDTA or enalaprilat. The pH optima for angiotensin II liberation were 4.0 for angiotensin I, 7.0 for angiotensinogen(1-14) fragment and 8.0 for angiotensinogen. The total amount of angiotensin II generating activity in the human submandibular gland is 5,000-times smaller than that in the rat gland.

Amino Acid Sequence↗
PubMed1988

Histological analysis of parotid and submandibular glands in chronic alcohol abuse: a necropsy study.

A quantitative histological analysis of the major salivary glands was carried out at necropsy in 28 alcoholics and in a series of age and sex matched controls. The findings were related to the different types of histologically diagnosed liver disease present. Significant quantitative changes of salivary gland structure were noted in cirrhosis but not in other forms of alcoholic liver disease. In cirrhotic subjects the parotid contained proportionally more adipose but less acinar tissues than in controls. The submandibular gland showed a proportional increase in adiposity and reduction in fibrovascular tissues but no noticeable reduction in its acinar proportional volume. Neither grossly detectable parotid enlargement nor acinar hypertrophy, a feature which has previously been noted as characteristic of alcoholic sialadenosis, were evident in this series. These findings provide little structural support for the reportedly increased secretory capacity of salivary glands in chronic alcohol abuse.

Adipose Tissue↗
PubMed1979

Histochemical study on the localization of glucose-6-phosphate dehydrogenase induced by androgen or thyroxine in the convoluted tubules of mouse submandibular gland.

The effects of 5 alpha-dihydrotestosterone (DHT) and thyroxine (T4) on glucose-6-phosphate dehydrogenase (G-6-PDH) activity in mouse submandibular gland were investigated histochemically. A strong positive histochemical reaction for G-6-PDH was observed in the excretory ducts of untreated male and female mice, with a slight reaction in the basal portion of the convoluted tubules (striated ducts) of males. Administration of DHT to female mice increased G-6-PDH activity specifically in the convoluted tubules. T4 increased the enzyme activity in the tubules more than DHT. The induction of G-6-PDH activity by T4 in adrenalectomized mice suggests that T4 has a direct effect on the submandibular gland.

Animals↗
PubMed1988

Quantitation and localization of acinar cell-specific mucin in submandibular glands of mice during postnatal development.

In this study, antiserum to acinar cell-specific mucin was utilized to determine whether mucin could be detected in the mouse submandibular gland prior to cytodifferentiation of acinar cells. Results from radioimmunoassay indicated that mucin occurs in submandibular glands from newborn mice, i.e., before the appearance of mature acinar cells. Additionally, mucin quantitated in various stages of development was found to be antigenically identical to adult mucin. After sections of glands were treated with immunohistochemical reagents, we observed that the mature acinar cell-specific mucin was present in secretory terminal-tubule cells and in proacinar cells of newborn animals. The present findings suggest that in young animals, the proacinar cells are an immediate precursor of acinar cells and that the secretory terminal-tubule cells may represent an earlier stage in development of acinar cells. In adult female glands, mucin was also detected in the granular intercalating-duct cells. This latter observation is consistent with the hypothesis that these cells are an intermediate in the acinar cell replacement process.

Aging↗
PubMed1987

Effects of monensin on the Na+ pump activity and the release of amylase and sialic acid in dog submandibular glands.

The effects of monensin on the Na+,K+-ATPase activity and the release of amylase and sialic acid were investigated in dog submandibular gland pieces. Monensin stimulated the Na+,K+-ATPase activity and amylase release in a dose-dependent manner. Moreover, this agent increased the Na+,K+-ATPase activity and the release of amylase and sialic acid induced by pilocarpine. These results suggest that monensin increases the release of amylase and sialic acid in dog submandibular glands, in part, through the Na+ pump activated due to the Na+ influx.

Amylases↗
PubMed2004

Expression and localization of the transcription factor JunD in the duct system of mouse submandibular gland.

We studied the expression and localization of JunD, a component of the transcription factor activator protein-1 (AP-1), in the mouse submandibular gland with immunoblotting and immunohistochemistry. In adult mice, all seven Jun and Fos family members constituting the AP-1 complex were expressed more abundantly in the female gland than in the male gland, and JunD was the most abundant of the members. Immunoreactivity for JunD was localized exclusively in the duct system of the gland, in which it was localized to the nuclei of intercalated duct (ID) cells and a subpopulation of striated duct (SD) cells located adjacent to ID. In contrast, granular convoluted tubule (GCT) cells, which are much more abundant in the male gland, were devoid of JunD. During postnatal development of the male gland, JunD was lost from the duct cells as they differentiated to GCT cells at 3-5 weeks postpartum. When GCT differentiation was induced in adult female gland by testosterone administration, many JunD-negative SD cells were temporarily induced to express JunD after 6-24 hr, but those cells lost JunD as they completely converted to GCT cells by 48 hr. These results suggested that JunD is involved in the differentiation of the duct system of mouse submandibular gland, in which there is crosstalk between the androgen/androgen receptor system and the AP-1 complex.

Animals↗
PubMed1996

Development of the submandibular gland and its closer neighboring structures in human embryos and fetuses of 19-67 mm CRL.

The fetal development and arrangement of the human submandibular gland was studied by means of serial sections of human embryos and fetuses ranging from 19 mm to 67 mm CRL. Computer assisted 3-dimensional reconstruction leads to the following observations: 1. The orifice of the submandibular duct is located in the medial paralingual sulcus. 2. There is evidence that the extension and location of WHARTON's duct is influenced by the surrounding structures. 3. The surface of the submandibular gland primordium shows impressions of the neighboring structures. 4. The glandular tissue is encapsulated in condensed mesenchyme.

Embryo, Mammalian↗
PubMed1990

Epidermal growth factor in serum, urine, submandibular glands and kidneys of diabetic mice.

Levels of epidermal growth factor (EGF) in serum were significantly decreased in streptozotocin (STZ)-diabetic mice (446 +/- 168 pg/ml after 1 week and 423 +/- 52 after 4 weeks vs 766 +/- 162 pg/ml in controls, P.002 and less than .001. respectively) and in genetically diabetic ob/ob mice (455 +/- 285 vs 962 +/- 453 pg/ml in nondiabetic ob/+ controls, P.043). The urinary excretion of EGF was significantly increased in STZ mice (104 +/- 53 vs 51 +/- 23 ng/h, P.013) but unchanged in ob/ob mice (33 +/- 9 vs 45 +/- 16 ng/h, P.134). However, when expressed per mg creatinine it was decreased in both cases: in STZ mice to 680 +/- 250 ng/mg at 1 week and 684 +/- 211 at 4 weeks vs 1250 +/- 303 ng/mg in controls (P less than .01); and in the ob/ob mice to 552 +/- 117 vs 1237 +/- 300 ng/mg in ob/+ controls (P less than .01). EGF content of the submandibular glands of STZ mice remained unchanged at 1 week (13.1 +/- 2.9 vs 11.0 +/- 1.8 micrograms/mg protein, P.170) but dropped by 4 weeks (4.7 +/- 1.2 micrograms/mg, P less than .001); in the ob/ob mice it was less than 20% that of controls (2.1 +/- 0.8 vs 12.2 +/- 3.6 micrograms/mg protein). In kidneys, the EGF content was not altered in either ob/ob (524 +/- 50 vs 571 +/- 33 pg/mg protein) or STZ mice (652 +/- 183 vs 665 +/- 80 pg/mg). The preproEGF mRNA level in STZ-treated mice was reduced after 4 weeks in submandibular glands but not in kidneys. The results show that diabetes affects EGF production, utilization and/or excretion in mice and that kidneys are spared from suppression of EGF synthesis that is pronounced in the submandibular glands.

Animals↗
PubMed2002

Kuttner tumor of the submandibular gland: fine-needle aspiration cytologic findings of seven cases.

Kuttner tumor or chronic sclerosing sialadenitis is a benign inflammatory condition of the submandibular gland that mimics a malignant neoplasm clinically because of presentation as a hard mass. This is an underrecognized entity in the surgical pathology and cytology literature. We describe thefine-needle aspiration cytologic findings of 7 cases with histologic correlation. The 6 men and 1 woman (age, 47-72 years) had unilateral (4 cases) or bilateral (3 cases) submandibular masses known to be present for 1 month to 6 years (mean, 15 months). The aspirates were paucicellular to moderately cellular. They were characterized by scattered tubular ductal structures often enveloped by collagen bundles or lymphoplasmacytic infiltrate, isolated fragments of fibrous stroma, a background rich in lymphoid cells, and paucity or absence of acini. Histologic examination of the excised submandibular glands revealed preserved lobular architecture, thickening of interlobular septa by sclerotic tissue, dense lymphoplasmacytic infiltrate, preservation of ducts with periductal fibrosis, and variable loss of acini. In combination with the clinical findings, the fine-needle aspiration cytologic findings can strongly suggest the diagnosis of Kuttner tumor and may obviate the need of surgical intervention.

Aged↗
PubMed1986

Induction of the synthesis of a specific protein in rat submandibular gland by isoproterenol.

Prolonged treatment of rats with the beta-adrenergic agonist, isoproterenol (IPR), produces hypertrophy and hyperplasia of the parotid and submandibular glands. The drug induces the synthesis of several secretory proteins that are absent or occur at very low concentrations in the gland or saliva of the untreated rat. We have measured the relative concentrations of one of these proteins (termed "large mobile" (LM) protein, Menaker et al. (1974) Lab. Invest. 30, 341-349) by using a solid phase enzyme-linked immunoabsorption assay. LM protein was not measurable in gland extracts of 20-day-old fetuses or 2-day-old rats. Its concentration was very low in the glands of 6- and 13-day-old and adult rats. Administration of IPR for 4 to 7 days to adult or 6-day old rats increased the levels of the LM protein by 20 to 25-fold. The LM protein was localized immunocytochemically primarily in the acinar cells in the glands of control and IPR-treated adult rats. In vitro translation studies using a mRNA-dependent reticulocyte lysate system and labeling with [35S]methionine showed: little synthesis of pro-LM from poly(A+) RNA from glands of adult rats and none from 13-day-old animals, and that, in comparison, poly(A+) RNA from glands of adult or 13-day-old IPR-treated rats directed the synthesis of a much greater concentration of pro-LM. The in vitro precursor of the LM protein migrated electrophoretically as a single band in anti-LM immunoprecipitates, and had a molecular weight of 14,000. The LM protein, which appears to be a single, unique polypeptide induced by IPR in the submandibular glands of developing and adult rats, will be useful in studies examining the effects of catecholamine beta-agonists on gene expression in an exocrine cell.

Animals↗
PubMed1994

Neuroendocrine regulation of inflammation and tissue repair by submandibular gland factors.

Interactions between the immune, nervous and endocrine systems are important in inflammation and tissue repair. One neuroendocrine pathway involves polypeptide factors derived from the submandibular glands, whose synthesis and release are controlled by cervical sympathetic nerves. This novel pathway of immune-neuroendocrine communication is the cervical sympathetic trunk-submandibular gland (CST-SMG) axis. Here, Ronald Mathison, Joseph Davison and Dean Befus discuss the contributions of this axis to the neuroendocrine regulation of inflammation and tissue repair.

Animals↗
PubMed1985

Effect of indomethacin on the bradykinin-induced vasodilation in the submandibular gland.

Effects of the local infusion of bradykinin or isoproterenol were studied on the systemic blood pressure, blood flow, and vascular resistance of the submandibular gland before and after indomethacin treatment in cats. Both bradykinin and isoproterenol were shown to potently increase the glandular perfusion rate. The systemic arterial blood pressure fell by about 20% in response to indomethacin. The enhancement of blood flow by bradykinin or isoproterenol was not, however, affected by indomethacin treatment. The present results appear to suggest that the endogenous prostaglandins are not essentially involved in the development of responses produced by bradykinin or isoproterenol in the cat submandibular gland.

Animals↗
PubMed2000

Reduction in carbonic anhydrase activity in the tongue epithelium and submandibular gland in zinc-deficient rats.

We investigated the effects of zinc deficiency on carbonic anhydrase (CA) activity in the tongue epithelium and submandibular gland in rats. Male 4-week-old SD rats were given free access to a diet containing 2.2 (zinc-deficient), 4.1 (low-zinc), or 33.7 (zinc-sufficient) mg zinc/kg diet for 6 weeks. Rats in the fourth group (receiving 33.7 mg zinc/kg) were pair-fed against the zinc-deficient rats. Biochemical analysis at the end of the experimental period indicated that zinc deficiency significantly reduced CA activity in the tongue epithelium and submandibular gland, and the CA activity levels in these tissues seemed to parallel the dietary zinc levels. By enzyme histochemistry, an intensely positive reaction for CA was observed in the middle and basal regions of the taste buds in the circumvallate papilla in the zinc-sufficient and pair-fed (control) rats. The cells in von Ebner's glands also showed a strong positive reaction in control rats, although only a weak reaction product was found in zinc-deficient rats. These results suggest that CA activity is affected by the dietary content of zinc, which is considered to be an indispensable factor for the maintenance of normal taste sensation.

Animal Feed↗
PubMedDate not supplied

Mucoepidermoid carcinoma expleomorphic adenoma of the submandibular gland.

We described a rare case of carcinoma expleomorphic adenoma in which mucoepidermoid carcinoma arise from a previous incompletely excised pleomorphic adenoma of the submandibular gland. The tumor was surgically resected along with a modified radical neck dissection and postoperative radiotherapy. The patient remained disease free 3 years after the last operation. The pathology showed concurrent presence of Warthin's tumor in the specimen. The concurrent presence of mucoepidermoid carcinoma, pleomorphic adenoma, and synchronous Warthin's tumor make this case unique, and such a combination associated with the submandibular gland has not been documented in the literature before.

Adenoma, Pleomorphic↗