Vasoactivity of the ventral aorta of the American eel (Anguilla rostrata), Atlantic hagfish ( Myxine glutinosa), and sea lamprey (Petromyzon marinus)

To determine if vascular smooth muscle from teleost and agnathan fishes expresses receptors for signaling agents that are important in vascular tension in other vertebrates, we exposed rings of aortic vascular smooth muscle from the eel (Anguilla rostrata), the hagfish (Myxine glutinosa), and the lamprey (Petromyzon marinus) to a suite of putative agonists, including: acetylcholine, endothelin, nitric oxide, natriuretic peptides, and prostanoids. Acetylcholine constricted aortic rings from the eel, but had no effect on the rings from lamprey. On the other hand, endothelin constricted rings from all three species. Use of receptor-specific ET agonists demonstrated that only ET(A) receptors are expressed in the eel and lamprey aorta. The nitric oxide donor sodium nitroprusside or nitric oxide itself dilated rings from the eel, but both agonists constricted rings from the hagfish and NO produced a biphasic response (constriction followed by dilation) in the lamprey. Two natriuretic peptides, eel ANP and porcine CNP, produced marginally significant dilation in the eel aorta, human ANP dilated the hagfish rings, and pCNP and eANP dilated the lamprey rings. The prostanoids PGE(1) and PGE(2) both dilated the eel aortic rings, and PGE(1) and carbaprostacyclin (stable PGI(2) agonist) dilated the hagfish and lamprey rings. Our results suggest that receptors for a variety of vasoactive signaling agents are expressed in the aortic smooth muscle of the earliest vertebrates (lamprey and hagfish), as well as the more advanced teleosts (eel).     

臭椿茎中分泌道的发育及其组织化学研究

利用植物解剖学方法研究臭椿茎和叶柄中分泌道的结构、分布和发育过程.结果表明:臭椿茎和叶柄中的分泌道分布于髓的周缘,次生木质部中无分泌道.分泌道是由一层分泌细胞围绕分泌腔而构成,分泌细胞外有1～2层鞘细胞.分泌道以裂生方式形成,其发育过程可分为3个阶段:原始细胞阶段、形成阶段和成熟阶段.在原始细胞阶段,一群原始细胞具浓厚细胞质,细胞核清晰可见;形成阶段,原始细胞的中央细胞间细胞壁中层降解,细胞壁分离,形成腔隙,随着分泌细胞数量的增加,分泌腔体积扩大;成熟阶段的分泌道具有12～16个分泌细胞,1～2层鞘细胞,分泌腔直径为30～50μm.组织化学研究表明,分泌细胞及分泌道内含物中含大量的萜类、多糖和脂类物质.机械创伤能够诱导次生木质部中产生创伤分泌道.臭椿茎中的分泌道和创伤性分泌道在抵御生物和非生物胁迫中起重要作用.     

Estrogen induced changes in Akt-dependent activation of endothelial nitric oxide synthase and vasodilation

OBJECTIVES: Acute administration of estrogen results in vasodilation and increased nitric oxide (NO) production. We examined the hypothesis that this is due to activation of Akt/PKB which subsequently increases eNOS activity. METHODS AND RESULTS: Treatment of bovine microvascular and human umbilical endothelial cells (HUVEC) with 17-beta-estradiol (E2) (10(-9) to 10(-5)M) increased phosphorylation of Akt within 1 min and this was followed by phosphorylation of eNOS. These effects were blocked by wortmannin, a PI(3)K inhibitor and the upstream activator of Akt. The estrogen receptor antagonist, ICI 182,780, inhibited eNOS phosphorylation. E2 increased calcium dependent NOS activity and nitrite production and this was inhibited by wortmannin and ICI 182,780. E2 increased the vasodilatory response of aortic rings to acetylcholine and wortmannin blocked the effect. E2 (10(-9)M) dilated cerebral microvascular vessels under conditions of no flow, constant flow and increasing flow and this was blocked by wortmannin. Tamoxifen, a partial estrogen receptor antagonist, also dilated the microvessels. CONCLUSIONS:: E2 increases NO production through an Akt/PKB dependent pathway. This is associated with increased sensitivity to endothelial dependent dilation. In cerebral microvessels, E2 and tamoxifen produce significant dilation at low concentrations with and without acetylcholine induced stimulation of endothelial vasodilation.     

Fine structure of the ventral and dorsal lobes of the prostate in the young adult Syrian hamster, Mesocricetus auratus

The normal ventral and dorsal prostatic lobes of the young adult Syrian hamster were examined at the light and electron microscopic levels. Each lobe is composed of branched tubular secretory units separated from each other by loose interacinar connective tissue and draining into the urethra. The lumen of each acinus is lined by a simple epithelium composed of columnar secretory cells with occasional small basal cells. The epithelial layer, with the thin underlying lamina propria, forms a mucosa that is often highly folded. The whole acinus is bounded by a thick muscular stroma. In each of the ventral lobes, there are three main ducts, each one formed of tubular branched tributary secretory units. The walls of the secretory acini are moderately folded. Microvilli dominate the lumenal surface of the secretory epithelial cells. The Golgi complex is very extensive and shows dilated cisternae and secretory vesicles and vacuoles of various sizes. Membrane-bounded secretory granules populate the Golgi and apical areas and are released into the acinar lumen by exocytosis. The rough endoplasmic reticulum is dispersed throughout the cytoplasm, except in the region of the Golgi apparatus. In each of the dorsal lobes, there are several main tubular ducts that open into the urethra. Both proximal (ductal) and distal portions of the glandular tree are secretory in nature. Microvilli and cytoplasmic bulges and blebs dominate the lumenal surface of the secretory cells. The cells are also characterized by highly dilated cisternae of rough endoplasmic reticulum. The secretory cells show heterogeneity in the degree of dilation and distribution of rough endoplasmic reticulum, and this heterogeneity may reflect location in the glandular tree.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of the epithelial layer in the generation of superoxide anion by the guinea-pig isolated trachea.

The lucigenin-dependent chemiluminescence generation by guinea-pig isolated tracheal two rings preparations was studied. Tracheal preparations stimulated with phorbol myristate acetate (PMA) or opsonized zymosan generated chemiluminescence. The total amount of chemiluminescence generated in 120 min was 754+/-63 mV x min for PMA and 4832+/-396 mV x min for zymosan. Generation of chemiluminescence was decreased by more than 50% when the tissues were co-incubated with superoxide dismutase (100 U/ml). Also, addition of direct donors of nitric oxide diminished chemiluminescence generation by zymosan-activated tracheal rings significantly by about 50%. However, the presence of the precursor or of inhibitors of nitric oxide synthase did not influence zymosan-induced chemiluminescence. Removal of the epithelial layer from tracheal rings caused an approximately 90% decrease in chemiluminescence response. However, isolated epithelial cell suspensions did not generate chemiluminescence. Histologic examination showed that the number of eosinophils in the tracheal tissue was reduced from 56+/-7 to 18+/-8 per mm basal membrane when the epithelial layer was removed. These results indicated that (1) superoxide anion formation can take place in the guinea-pig trachea, (2) eosinophils in the epithelial and submucosal layers of guinea-pig trachea are likely candidates for superoxide generation although other cell types can also be involved, and (3) besides relaxing airway smooth muscle, nitric oxide donors may also affect superoxide in the airways.     

Vasodilator mechanisms in the dorsal aorta of the giant shovelnose ray, Rhinobatus typus (Rajiformes; Rhinobatidae)

This study investigated the nature of vasodilator mechanisms in the dorsal aorta of the giant shovelnose ray, Rhinobatus typus. Anatomical techniques found no evidence for an endothelial nitric oxide synthase, but neural nitric oxide synthase was found to be present in the perivascular nerve fibres of the dorsal aorta and other arteries and veins using both NADPH-diaphorase staining and immunohistochemistry with a specific neural NOS antibody. Arteries and veins both contained large nNOS-positive nerve trunks from which smaller nNOS-positive bundles branched and formed a plexus in the vessel wall. Single, varicose nNOS-positive nerve fibres were present in both arteries and veins. Within the large bundles of both arteries and veins, groups of nNOS-positive cell bodies forming microganglia were observed. Double-labelling immunohistochemistry using an antibody to tyrosine hydroxylase showed that nearly all the NOS nerves were not sympathetic. Acetylcholine always caused constriction of isolated rings of the dorsal aorta and the nitric oxide donor, sodium nitroprusside, did not mediate any dilation. Addition of nicotine (3 x 10(-4) M) to preconstricted rings caused a vasodilation that was not affected by the nitric oxide synthase inhibitor, L-NNA (10(-4) M), nor the soluble guanylyl cyclase inhibitor, ODQ (10(-5) M). This nicotine-mediated vasodilation was, therefore, not due to the synthesis and release of NO. Disruption of the endothelium significantly reduced or eliminated the nicotine-mediated vasodilation. In addition, indomethacin (10(-5) M), an inhibitor of cyclooxygenases, significantly increased the time period to maximal dilation and reduced, but did not completely inhibit the nicotine-mediated vasodilation. These data support the hypothesis that a prostaglandin is released from the vascular endothelium of a batoid ray, as has been described previously in other groups of fishes. The function of the nitrergic innervation of the blood vessels is not known because nitric oxide does not appear to regulate vascular tone.     

Fasciola hepatica: Azetidine inhibition of bile duct hyperplasia in the infected rat

In controlled experiments the luminal bile duct perimeters were compared between rats infused with l-azetidine-2-carboxylic acid (AZC) (120 μmole/rat/day) and rats infused with saline after both groups had been implanted with adult Fasciola. The average bile duct lumen in the group receiving AZC did not enlarge relative to controls, and was about one-half the average perimeter of ducts from rats infused with saline that had worm implants. These results indicate that azetidine can inhibit bile duct hyperplasia induced by Fasciola which inhabit the duct. The results also support the hypothesis that the hyperplasia of fascioliasis is mediated through the release of free proline from the worms where it is present in high concentrations.     

Dietary obesity increases NO and inhibits BKCa-mediated, endothelium-dependent dilation in rat cremaster muscle artery: association with caveolins and caveolae

Obesity is a risk factor for hypertension and other vascular disease. The aim of this study was to examine the effect of diet-induced obesity on endothelium-dependent dilation of rat cremaster muscle arterioles. Male Sprague-Dawley rats (213 ± 1 g) were fed a cafeteria-style high-fat or control diet for 16-20 wk. Control rats weighed 558 ± 7 g compared with obese rats 762 ± 12 g (n = 52-56; P < 0.05). Diet-induced obesity had no effect on acetylcholine (ACh)-induced dilation of isolated, pressurized (70 mmHg) arterioles, but sodium nitroprusside (SNP)-induced vasodilation was enhanced. ACh-induced dilation of arterioles from control rats was abolished by a combination of the K(Ca) blockers apamin, 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34), and iberiotoxin (IBTX; all 0.1 μmol/l), with no apparent role for nitric oxide (NO). In arterioles from obese rats, however, IBTX had no effect on responses to ACh while the NO synthase (NOS)/guanylate cyclase inhibitors N(ω)-nitro-L-arginine methyl ester (L-NAME; 100 μmol/l)/1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 μmol/l) partially inhibited ACh-induced dilation. Furthermore, NOS activity (but not endothelial NOS expression) was increased in arteries from obese rats. L-NAME/ODQ alone or removal of the endothelium constricted arterioles from obese but not control rats. Expression of caveolin-1 and -2 oligomers (but not monomers or caveolin-3) was increased in arterioles from obese rats. The number of caveolae was reduced in the endothelium of arteries, and caveolae density was increased at the ends of smooth muscle cells from obese rats. Diet-induced obesity abolished the contribution of large-conductance Ca(2+)-activated K(+) channel to ACh-mediated endothelium-dependent dilation of rat cremaster muscle arterioles, while increasing NOS activity and inducing an NO-dependent component.     

Glutamine-dependent inhibition of pial arteriolar dilation to acetylcholine with and without hyperammonemia in the rat

Glutamine has been shown to influence endothelial-dependent relaxation and nitric oxide production in vitro, possibly by limiting arginine availability, but its effects in vivo have not been well studied. Hyperammonemia is a pathophysiological condition in which glutamine is elevated and contributes to depressed CO(2) reactivity of cerebral arterioles. We tested the hypothesis that acute hyperammonemia decreases pial arteriolar dilation to acetylcholine in vivo and that this decrease could be prevented by inhibiting glutamine synthetase with L-methionine-S-sulfoximine (MSO) or by intravenous infusion of L-arginine. Pial arteriolar diameter responses to topical superfusion of acetylcholine were measured in anesthetized rats before and at 6 h of infusion of either sodium or ammonium acetate. Ammonium acetate infusion increased plasma ammonia concentration from approximately 30 to approximately 600 microM and increased cerebral glutamine concentration fourfold. Arteriolar dilation to acetylcholine was intact after infusion of sodium acetate in groups pretreated with vehicle or with MSO plus methionine, which was coadministered to prevent MSO-induced seizures. In contrast, dilation in response to acetylcholine was completely blocked in hyperammonemic groups pretreated with vehicle or methionine alone. However, MSO plus methionine administration before hyperammonemia, which maintained cerebral glutamine concentration at control values, preserved acetylcholine dilation. Intravenous infusion of L-arginine during the last 2 h of the ammonium acetate infusion partially restored dilation to acetylcholine without reducing cerebral glutamine accumulation. Superfusion of 1 or 2 mM L-glutamine through the cranial window for 1 h in the absence of hyperammonemia attenuated acetylcholine dilation but had no effect on endothelial-independent dilation to nitroprusside. We conclude that 1) hyperammonemia reduces acetylcholine-evoked dilation in cerebral arterioles, 2) this reduction depends on increased glutamine rather than ammonium ions, and 3) increasing arginine partially overcomes the inhibitory effect of glutamine.     

Adenosine and hypoxic dilation of rat coronary small arteries: roles of the ATP-sensitive potassium channel, endothelium, and nitric oxide

The aims of the study were to examine the roles of the ATP-sensitive potassium (K(ATP)) channel, the endothelium, and nitric oxide (NO) in the responses of rat coronary small arteries to adenosine and hypoxia. Segments of rat coronary vessel were investigated in vitro using pressure myography; all vessels studied developed stable spontaneous myogenic tone during equilibration. Glibenclamide (a K(ATP) channel inhibitor) reversed pinacidil but not 2-deoxyglucose-induced dilation. Both adenosine and hypoxia dilated the vessels, and glibenclamide did not reverse these responses. Endothelial removal or N(G)-nitro-L-arginine methyl ester (L-NAME) inhibited the dilation to adenosine by approximately 50%; subsequent addition of glibenclamide was without effect. Hypoxic dilation was completely inhibited by endothelium removal or L-NAME. We conclude that adenosine- and hypoxia-induced dilation of rat coronary arteries does not appear to involve the K(ATP) channel. Adenosine-induced dilation is partially and hypoxic dilation is completely dependent on endothelium-derived NO.     

Dopamine-induced epithelial K(+) and Na(+) movements in the salivary ducts of Periplaneta americana

K(+)- and Na(+)-selective double-barrelled microelectrodes were used for intracellular and luminal measurements in salivary ducts of Periplaneta americana. The salivary ducts were stimulated with dopamine (10(-6) mol l(-1)). Dopamine decreased intracellular [K(+)] from 112+/-17 mmol l(-1) to 40+/-13 mmol l(-1) (n=6) and increased intracellular [Na(+)] from 22+/-19 mmol l(-1) to 92+/-4 mmol l(-1) (n=6). Luminal [K(+)] was 15+/-3 mmol l(-1) in the unstimulated salivary ducts and increased to 26+/-11 mmol l(-1) upon stimulation with dopamine (n=10). Luminal [Na(+)] was insignificantly increased from 105+/-25 mmol l(-1) to 116+/-22 mmol l(-1) (n=12) by stimulation with dopamine. The potential difference across the basolateral membrane (PD(b)) was depolarized from -65+/-6 mV to -31+/-13 mV (n=12) and the transepithelial potential difference (PD(t)) was hyperpolarized from -13+/-6 mV to -22+/-7 mV (n=22, lumen negative) upon stimulation with dopamine. The re-establishment of prestimulus values of intracellular [K(+)] and [Na(+)] and PD(b) was inhibited by basolateral addition of ouabain (10(-4) mol l(-1)). Furosemide (10(-4) mol l(-1)) in the bath inhibited the dopamine-induced increase in intracellular [Na(+)], the decrease in intracellular [K(+)] and the depolarization of PD(b). We propose a model for dopamine-stimulated ion transport in the salivary ducts involving basolateral Na(+)-K(+)-2Cl(-) cotransport and active extrusion of K(+) via the apical membrane.     

Taurine attenuates lipopolysaccharide-induced disfunction in mouse mammary epithelial cells

The intent of this study was to evaluate the active defense reaction of mouse mammary epithelial cells and the cytoprotective and anti-inflammatory properties of taurine to lipopolysaccharide (LPS)-induced disfunction in mouse mammary epithelial cells. (1) Primary cultured mouse mammary epithelial cells were stimulated with LPS for 24 h (final concentration=0, 5, 10, 20 μg/mL). Western blotting demonstrated a significant decrease in the secretion of β-casein in the 20 μg/mL LPS treatment group (P<0.05), while nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), lactoferrin (LF) and N-acetyl-β-D-glucosaminidase (NAGase) were all significantly increased following LPS treatment (P<0.01). Furthermore, cell survival was significantly inhibited after treatment with 20 μg/mL LPS; however, neither 5 μg/mL nor 10 μg/mL LPS had any effect on cell survival. Therefore, a level of 10 μg/mL LPS was selected to test the protective effect of taurine on mouse mammary epithelial cells. (2) Primary cultured mouse mammary epithelial cells were treated with 0, 5, 15 or 45 mmol/L taurine for 3 h, followed by 10 μg/mL LPS for 24 h. Taurine significantly attenuated the LPS-induced increase in NAGase activity, NO concentrations and the level of TNF-α, IL-1β, IL-6 and LF. Taurine at 45 mmol/L markedly increased β-casein secretion in response to LPS-induced disfunction. This study demonstrated that the addition of taurine to a culture medium significantly inhibited the LPS-induced release of inflammatory factors and increased β-casein secretion from mammary epithelial cells, thereby providing a possible explanation for the protective effect proposed for taurine in the prevention of LPS-induced disfunction in mammary epithelial cells.     

Changes in the main submandibular salivary duct of rabbits resulting from ductal ligation

Normal submandibular ducts from rabbits have been examined by mucosubstance histochemistry, transmission and scanning electron microscopy. The results were compared with the appearances of ducts removed 4...6 weeks after ligation. The normal ducts were composed mainly of columnar "light" cells and basal cells but, in addition, some "dark" cells and scattered goblet containing sulphated mucins were always present. The luminal surface of the ductal cells possessed numerous microvilli protruding into the lumen, and a rim of negatively charged mucin was present on this surface of these cells. After ligation the ducts became greatly distended by their fluid contents which remained under pressure until the duct was incised. The epithelial cells were flattened and appeared to contain less cytoplasm per cell; "light" cells, basal cells and "dark" cells were still recognisable. Goblet cells were much more plentiful than in the control ducts and often protruded into the lumen despite the increased intraluminal pressure. The development of a number of ciliated cells had also occurred and they were often situated close to goblet cells. Lymphatic vessels were more prominent around the ligated ducts. Luminal microvilli were less numerous than in the control ducts but the rim of negatively charged mucin on the luminal surface of ductal cells was more conspicuous. Mixed inflammatory cells were present within the lumina of ligated ducts especially in those parts adjacent to the ductal cells. No inflammatory cell has been observed passing through the wall of a main duct and the possibility exists that these cells had entered lumina within the gland and migrated from there to the main duct. The above findings may serve to help our understanding or physiological events in the ducts.     

Expression of constitutively active Notch1 in male genital tracts results in ectopic growth and blockage of efferent ducts, epididymal hyperplasia and sterility

The Notch signaling pathway is involved in a variety of developmental processes. Here, we characterize the phenotypes developing in the reproductive organs of male transgenic (Tg) mice constitutively expressing the activated mouse Notch1 intracellular domain (Notch1(intra)) under the regulatory control of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR). Tg expression was detected in testis, vas deferens and epididymis by Northern blot analysis. In situ hybridization with a Notch1-specific probe lacked sensitivity to detect expression in normal-appearing cells, but demonstrated expression in hyperplastic epithelial cells of the vas deferens, epididymis and efferent ducts. Tg males from three independent founder lines were sterile. Histological analysis of reproductive organs of young Tg males (postnatal ages 8 and 21) showed no difference compared to those of non-Tg males. In contrast, in adult Tg mice from day 38 onwards, the efferent ducts, the vas deferens and most epididymal segments revealed bilateral epithelial cell hyperplasia with absence of fully differentiated epithelial cells. Electron microscopy confirmed the uniformly undifferentiated state of these cells. Immunohistochemistry with anti-PCNA antibody also revealed enhanced proliferation of Tg epididymis. In adult Tg testis, the different generations of germ cells of seminiferous tubules appeared normal, although some tubules were highly dilated and revealed an absence of early and/or late spermatids. The epithelial cells of the Tg tubuli recti and rete testis were not abnormal, but the rete testis was highly dilated and contained numerous spermatozoa, suggesting a downstream blockage. Consistent with a blockage of efferent ducts often seen at the rete testis/efferent duct interface, spermatozoa were absent in epididymis of all adult Tg mice and in all highly hyperplastic efferent duct tubules of these Tg mice. Such a blockage was visualized by injection of Evans blue dye into the rete testis lumen. Finally, the presence of ectopic hyperplastic efferent duct tubules was observed within the testicular parenchyma itself, outside their normal territory, suggesting that Notch1 signaling is involved in the establishment of these borders. This phenotype seems to represent a novel developmental defect in mammals. Together, these results show that constitutive Notch1 signaling significantly affects the development of male reproductive organs.     

An ultrastructural analysis of the salivary system of the terrestrial mollusc, Limax maximus.

The bilateral salivary glands, ducts, and nerves of the giant garden slug Limax maximus control the secretion of saliva and its transport to the buccal mass. Each salivary nerve, which originates at the buccal ganglion, contains over 3000 axon profiles. The axons innervate the musculature of the duct and branch within the gland. The salivary duct is composed of several muscular layers surrounding an epithelial layer which lines the duct lumen. The morphology of the duct epithelium indicates that it may function in ion or water balance. The salivary gland contains four major types of secretory cells. The secretory products are released from vacuoles in the gland cells, and are presumably transported by cilia in the collecting ducts of the gland into the larger muscular ducts.     

Role of cGMP in carbon monoxide-induced cerebral vasodilation in piglets

The hypothesis was addressed that CO-induced cerebral vasodilation requires a permissive cGMP signal that can be produced by nitric oxide (NO). Anesthetized piglets were implanted with cranial windows for measurement of pial arteriolar responses to stimuli. Pial arterioles dilated in response to isoproterenol (Iso), sodium nitroprusside (SNP), and CO or the CO-releasing molecule Mn2(CO)10 [dimanganese decacarbonyl (DMDC)]. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a soluble guanylyl cyclase inhibitor, decreased cerebrospinal fluid (CSF) cGMP and selectively inhibited dilations to SNP and DMDC without affecting the dilation to Iso. However, DMDC did not cause an increase in cortical periarachnoid CSF cGMP concentration. cGMP clamp with a threshold dilator level of 8-bromo-cGMP (10(-4) M) and ODQ restored the dilation to DMDC that had been blocked by ODQ alone. Under these conditions, cGMP was present but could not increase. Inhibition of the pial arteriolar dilation to glutamate by N-nitro-l-arginine, which blocks NO synthase, was similar to that by heme oxygenase inhibitors, which block endogenous CO production. The dilation to glutamate, similar to dilation to DMDC, was partially restored by 8-bromo-cGMP and completely restored by SNP (5 x 10(-7) M). These data suggest that the permissive role of NO in CO- and glutamate-induced vasodilation involves maintaining the minimum necessary cellular level of cGMP to allow CO to cause dilation independently of increasing cGMP.     

Morphological development of the swim bladder in hatchery-reared striped trumpeter Latris lineata

This study examined swim bladder morphogenesis in three cohorts of striped trumpeter (Latris lineata), a euphysoclist species with physostomous larvae. The swim bladder was first discernible 1–2 days after hatching as an evagination on the dorsal surface of the incipient digestive tract. It comprised a cluster of mesenchymal cells surrounding an inner primordium of epithelial cells. At mouth opening in larvae of 5.3 mm standard length (SL), the swim bladder was noticeably enlarged. Histologically, the swim bladder lumen was dilated and liquid filled. The pneumatic duct was first seen during the dilation stage and the rete mirabile began forming among the connective tissue surrounding the swim bladder. Initial swim bladder inflation occurred on day 11 post‐hatching in Cohort 1, at 14°C, and day 9 post‐hatching, in Cohorts 2 and 3, at 16°C. Histologically, the lumens of inflated swim bladders were ellipsoid and the epithelium was squamous, except for cuboidal gas gland cells at the anterio‐ventral and anterio‐lateral regions of the swim bladder. During the initial inflation interval the pneumatic duct was dilated in larvae both with and without swim bladder inflation. The pneumatic duct began to regress in some larvae over 7.5 mm SL. The swim bladder of striped trumpeter was similar to larvae of other altricial perciform marine fish in respect to organ derivation, tissue differentiation, luminal dilation and initial gaseous inflation. However, variations, particularly the delay in initial swim bladder inflation until after the start of feeding, were observed that could be fundamental to problems encountered during larval rearing.     

Distribution, Development and Structure of Resin Ducts in Guayule (Parthenium argentatum Gray)

The distribution, development and structure of resin ducts inguayule (Parthenium argentatum Gray), the second best sourceof natural rubber, have been studied. Resin ducts are widelydistributed in stem, root, leaf, petiole and peduncle. The ductsin the primary tissues are initiated schizogenously and theirfurther development is schizolysigenous. The ducts in the cortexof the root do not have a well-defined epithelium. Ducts developedfrom the vascular cambium are initiated and develop schizogenously.Both resin and rubber are produced in the epithelial cells ofresin ducts. While resin is secreted into the duct lumen, rubberis stored within these cells. Epithelial cells store more thanneighbouring parenchyma cells. Guayule, rubber, resin, ducts, epithelial cells     

ULTRASTRUCTURE OF THE SECRETORY DUCTS OF RHUS GLABRA L.

The infrastructure and development of the secretory ducts were studied in the secondary phloem of Rhus glabra L. The ducts were found to develop schizogenously. The electron microscope observations may explain the view of several previous authors of schizo-lysigenous development of the duct lumen in the Anacardiaceae. The secreted material consists of lipophilic and polysaccharide substances. The electron micrographs suggest that the lipophilic substances arise in plastids, ER cisternae, Golgi vesicles, and mitochondria. The polysaccharide constituents apparently originate from the outer wall layers of the epithelial cells. The wall layers facing the lumen of the duct disintegrate and form, together with the secreted osmiophilic droplets, the gum-resin. Numerous microtubules were found along walls of the epithelial cells.