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  • 1
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; impotence ; prostacyclin ; penis rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In view of the marked increase in blood flow into the penis during erection and the association of diabetes mellitus with impotence, we used the diabetic rat model to investigate the possibility that: (a) the penis may produce prostacyclin; and (b) prostacyclin secretion may be decreased in diabetes. Rats given a high dose of streptozotocin (120 mg/kg body weight) developed acute ketotic diabetes and were killed after 48 h. Animals given a low dose of streptozotocin (65 mg/ kg body weight) developed non-ketonuric diabetes and were killed after 7 or 62 days. Aortic rings and penile tissue discs were incubated in buffer, which was assayed for 6-oxo-pros-taglandin F1α, the stable and spontaneous breakdown product of prostacyclin. Penile tissue from control, ketotic and non-ketonuric (7 days) animals released similar quantities of prostacyclin, whereas that from long-term non-ketonuric animals (62 days) produced significantly less prostacyclin. Production of this prostanoid by the aortic rings paralleled these changes. We conclude that: (a) penile tissue releases prostacyclin in quantities comparable to those of the aorta; (b) long-term diabetes leads to diminished prostacyclin release by penile and aortic tissue: the former may contribute to the pathogenesis of diabetic impotence; and (c) since short-term ketotic diabetes does not inhibit aortic or penile prostacyclin release, duration of diabetes rather than its severity is responsible for diminished prostacyclin release.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Prostacyclin ; Thromboxane A2 ; Small intestine ; Mesenteric vasculature ; Fasting ; Semistarvation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The synthesis of prostacyclin (PGI2) and thromboxane A2 (TXA2) by the mucosal and muscular portions of the duodenum, jejunum, ileum and ascending colon, as well as that by mesenteric vessels, was investigated in starved and semistarved rats. The jejunal mucosa and muscularis showed a marked increase in PGI2 synthesis after fasting for 48 h and 72 h or semistarvation for 9 days when compared with controls. Jejunal TXA2 synthesis did not alter. In contrast, PGI2 and TXA2 synthesis in ileal mucosa and muscularis was significantly reduced after fasting for 48 h, 72 h and semistarvation for 9 days. PGI2 and TXA2 synthesis by duodenal and colonic muscularis was unaffected by fasting or semistarvation. PGI2 synthesis in mesenteric vessels was significantly increased by fasting and semistarvation. No changes in PGI2 or TXA2 were detected at 24 h in fasted rats in any of the tissues studied when compared with controls. These selective changes in PGI2/TXA2 secretion may be important mediators of adaptive changes in the small intestine in response to starvation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1434-0879
    Keywords: Key words Diabetic cystopathy ; Rabbit ; Cyclic AMP ; Cyclic GMP ; Prostacyclin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dysfunction of the urinary bladder is a recognised complication of diabetes mellitus (DM) which has been attributed, in part, to a direct effect on bladder smooth muscle tissue. The objective of this study was to investigate the effect of alloxan-induced DM on endogenous modulators of smooth muscle tone such as cyclic AMP (cAMP), cyclic GMP (cGMP) and prostaglandins. Male New Zealand white rabbits were rendered diabetic (hyperosmolar, non-ketotic) with an i.v. injection of alloxan. After 6 months, the urinary bladders and urethrae were excised, cut into segments, incubated with stimulators and the formation of prostaglandins (PG), cAMP and cGMP measured using radioimmunoassays. PGE2 and PGI2 formation was impaired in response to arachidonic acid stimulation, whereas it was increased in response to acetylcholine in DM detrusor, bladder neck and urethra compared to controls. Cyclic AMP and cGMP formation in response to forskolin and sodium nitroprusside, respectively, was significantly reduced in the DM tissues of the lower urinary tract compared to the control. Alterations in the formation of prostaglandins, cAMP and cGMP by the smooth muscle of DM lower urinary tract suggests that these biochemical mediators may have a pathophysiological role in the urinary bladder dysfunction associated with DM.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1434-0879
    Keywords: Key words Endothelin receptors ; Nitric oxide synthase ; Rabbit ; Bladder obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bladder outlet obstruction (BOO) is associated with altered bladder structure and function. Endothelin-1 (ET-1) has mitogenic and potent contractile properties. There are two ET receptors: ETA and ETB. Nitric oxide synthase (NOS) is the enzyme responsible for the synthesis of nitric oxide (NO) which is involved in smooth muscle relaxation. We investigated whether there are any changes in the density of ET-receptors and NOS in the detrusor and bladder neck in a rabbit model of BOO. Partial BOO was induced in adult male New Zealand White rabbits. Sham operated age-matched rabbits acted as controls. After six weeks the urinary bladders were excised and detrusor and bladder neck sections incubated with radioligands for ET-1, ETA and ETB receptors and with [3H]–l-NOARG (a ligand for NOS). NADPH histochemistry was also performed. BOO bladder weights were significantly increased (P=0.002). ET-1 binding and ETA receptor binding sites were significantly increased in the BOO detrusor smooth muscle (P=0.04, P=0.03 respectively) and urothelium (P=0.002, P=0.02 respectively). ETB receptor binding sites were also significantly increased in the BOO detrusor smooth muscle (P=0.04). However, there was no change in the BOO bladder neck. NOS was significantly decreased in the detrusor smooth muscle (P=0.003) and urothelium (P=0.0002). In the bladder neck NOS was also significantly reduced in the urothelium (P=0.003). NADPH staining was decreased in the detrusor and bladder neck. The up-regulation of ET receptors along with the down-regulation of NOS in the detrusor may contribute to the symptoms associated with BOO. Since ET-1 has a mitogenic role, especially via its ETA receptors, the increase in ETA receptors may also be involved in detrusor hyperplasia and hypertrophy in BOO. ET antagonists may therefore have a role in the treatment of patients with BOO.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1434-0879
    Keywords: Key words Endothelin-1 ; Rabbit ; Bladder ; Diabetes mellitus ; Smooth muscle cell proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary bladder hypertrophy and hyperplasia are well recognised in diabetic cystopathy. The urinary bladder is known to synthesise endothelin-1 (ET-1), a potent vasoconstrictor peptide with mitogenic properties. Using diabetic New Zealand White (NZW) rabbits, we investigated the potential role of ET receptor subtypes (ETA and ETB) on the proliferation of bladder smooth muscle cells (SMC). Diabetes mellitus was induced in adult male NZW rabbits. After 6 months, control (n=6) and diabetic (n=6) bladders were removed and SMC from the dome and bladder neck were grown using standard explant methodology. At passage two, the cells were made quiescent and then further incubated in foetal calf serum (FCS), control age-matched rabbit serum (CRS) or diabetic rabbit serum (DRS) in the presence or absence of ETA-antagonist (BQ123) or ETB-antagonist (BQ788). SMC proliferation was then measured with 5-bromo-2′deoxy-uracil 24 h later and by cell counting (using a haemocytometer) at 48 h. Neither BQ123 nor BQ788 influenced detrusor or bladder neck SMC proliferation in FCS or CRS. However, in the presence of DRS, BQ123 and BQ788 significantly inhibited diabetic detrusor and bladder neck SMC proliferation at 30 and 100 nmol/l (P 〈 0.03 and P 〈 0.01, respectively). Cell counts were also significantly reduced from the diabetic detrusor and bladder neck (P 〈 0.01 and P 〈 0.03 with BQ123 and BQ788, respectively). These results suggest that ET may play a pathophysiological role in the bladder SMC hyperplasia associated with diabetes mellitus.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 42 (1986), S. 945-948 
    ISSN: 1420-9071
    Keywords: Intestine ; adaptation ; absorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary We report here the effects of a 72-h fast on the localisation of Na-dependent [3H]-valine uptake by rat small intestine. Starvation results in the earlier appearance of valine transport during cell migration and an enhanced accumulation of the amino acid at the villus tip.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurocytology 13 (1984), S. 267-280 
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Uptake of horseradish peroxidase was studied by examining percentages of labelled synaptic vesicles in nerve endings of the excitatory axon innervating the opener muscle of the walking leg in the crayfish (Procambarus clarkii). Terminals on fibres with large excitatory postsynaptic potentials (EPSP) had higher percentage of labelled vesicles than terminals of fibres with small EJPs. The extent of labelling in the synaptic vesicle pool was greater for terminals with higher transmitter output. Evidence for three possible routes of synaptic vesicle formation was found. Movement of vesicles within the terminal as a whole appeared to be constrained, but rapid movement of vesicles within local populations probably occurs.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-136X
    Keywords: Octopamine ; Juvenile hormone ; cAMP ; Cockroach ; Electrophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Juvenile hormone production by the corpora allata of the adult female cockroach, Diploptera punctata, can be modulated by treatment with the biogenic amine, octopamine. Endogenous octopamine has been identified within the CA, using HPLC and electrochemical detection. Treatment with octopamine results in a sinusoidal, dose-dependent inhibition of JH biosynthesis by CA from day 2 virgin females, with maximal inhibition occurring at 10-10 M and 10-4 M. In day 4 and day 8 mated female corpora allata octopamine inhibited JH biosynthesis at 5·10-5 M. Although the elevation of either cAMP or cGMP within the CA is known to be associated with an inhibition of JH biosynthesis, treatment with high concentrations of octopamine results in an increase in the level of cAMP but not cGMP. This effect is both dose- and time-dependent. Octopamine treatment also initiates changes in the passive membrane responses of the CA. Superfusion of CA with octopamine results in a pronounced hyperpolarization of CA cells and an increase in the electrotonic potential (indicative of the degree of electrical coupling between CA cells). This effect could be blocked by the octopamine receptor blocker phentolamine. Treatment with octopamine or phentolamine also blocked the hyperpolarization of CA cells normally associated with electrical stimulation of the axon tracts innervating the CA. We hypothesize that octopamine may be a natural neuromodulator of JH production by CA, regulating ion channels in CA cells themselves as well as release of the inhibitory neuropeptide, allatostatin, from the terminals within the CA.
    Type of Medium: Electronic Resource
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