Biomedical subjects

H E Moss

Publications and source records attributed to H E Moss.

9 recordsLinked to original sources

PubMed1992

Loss of sensory neuropeptides in the obstructed human bladder.

This is the first investigation of alterations in the innervation of the obstructed human bladder by nerves containing neuropeptides. The patient groups studied were those with stable detrusor function, those with unstable detrusor function, and those presenting with acute retention of urine. Specimens of bladder tissue were taken from the lateral wall of the bladder below the peritoneal reflection. A total of 23 patients was studied (control, n = 4; acute retention, n = 5; stable obstruction, n = 5; unstable obstruction, n = 9). Substance P, calcitonin gene-related peptide and vasoactive intestinal polypeptide levels in the bladder were quantified by immunoassay. The density of innervation of the bladder detrusor by nerves containing these neurotransmitters and by those containing neuropeptide Y and somatostatin was assessed using both semiquantitative and quantitative immunohistochemical techniques. A reduction in the density of innervation by vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and somatostatin-immunoreactive but not neuropeptide Y-immunoreactive nerve fibres was shown in the obstructed bladder. These findings, combined with the significant reduction in substance P content of the obstructed bladder and in particular of the acute retention bladder, indicate that there may be an afferent nerve dysfunction resulting from prostatic bladder outflow obstruction.

Aged↗

PubMed1991

Patients with lower motor spinal cord lesion: a decrease of vasoactive intestinal polypeptide, calcitonin gene-related peptide and substance P, but not neuropeptide Y and somatostatin-immunoreactive nerves in the detrusor muscle of the bladder.

Specimens of the detrusor muscle of the bladder from four patients with lower motor neurone lesion and three patients with carcinoma of the bladder used as "controls", were studied immunohistochemically for vasoactive intestinal polypeptide, neuropeptide Y, calcitonin-gene related peptide, substance P and somatostatin. The greatest density of nerves in the bladder from "control" patients contained neuropeptide Y, followed in a decreasing order by vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and somatostatin. Neuropeptide Y- and vasoactive intestinal polypeptide-immunoreactive nerves were found throughout the smooth muscle and the base of the mucosa, while calcitonin gene-related peptide-, substance P- and somatostatin-immunoreactive nerves were found predominantly in nerve bundles with a few single fibres at the base of the mucosa. Vasoactive intestinal polypeptide-, neuropeptide Y- and calcitonin gene-related peptide-immunoreactive nerves were also located around blood vessels. In patients with lower motor neurone lesion, there was a decrease in the density of vasoactive intestinal polypeptide-, calcitonin gene-related peptide- and substance P-immunoreactive nerves, but there was little change in neuropeptide Y- or somatostatin-immunoreactive nerves. Urinary retention, bladder areflexia and deficient sensation may be directly linked to neuropeptide neuropathy in patients with lower motor neurone lesion.

Adult↗

PubMed1990

Neuropeptide immunoreactivity and choline acetyltransferase activity in the mouse urinary bladder following inoculation with Semliki Forest Virus.

The effect of Semliki Forest Virus, a known central demyelinating agent and a proposed model for multiple sclerosis, on the innervation of the mouse urinary bladder has been examined 3, 6, 9 and 12 weeks after inoculation. Three weeks after Semliki Forest Virus inoculation, vasoactive intestinal polypeptide content of the bladder was reduced and the density of vasoactive intestinal polypeptide-immunoreactive nerves was decreased in the smooth muscle, but not in the mucosa. Choline acetyltransferase activity and neuropeptide Y and substance P content was normal, as was the pattern of innervation by acetylcholinesterase-containing and neuropeptide Y- and substance P-immunoreactive nerve fibres. Six weeks after Semliki Forest Virus inoculation, the choline acetyltransferase activity was significantly reduced. Between 6 and 9 weeks the level of vasoactive intestinal polypeptide in the bladder of Semliki Forest Virus-infected mice significantly increased, so that at 9 weeks it was higher than the control value. However, by 12 weeks both choline acetyltransferase activity and vasoactive intestinal polypeptide content were normal. At this time, the substantial age-related increase in substance P content of the bladder was more pronounced in the Semliki Forest Virus-treated animals. Thus there are transitory changes in the innervation of the mouse bladder by vasoactive intestinal polypeptide-containing and cholinergic nerve fibres after exposure to a central demyelinating agent which may reflect changes in bladder dysfunction seen in multiple sclerosis patients.

Animals↗

PubMed1990

The effects of granisetron, ICS 205-930 and ondansetron on the visceral pain reflex induced by duodenal distension.

1. Distension of the duodenum in anaesthetized rats, by rapid application of intraluminal pressures (10-75 cmH2O), evoked falls in diastolic blood pressure and intragastric pressure. 2. The distension-induced responses were blocked by pretreatment with morphine (20 mg kg-1, s.c.), an action reversible by injection of naloxone (5 mg kg-1, i.v.). 3. Bilateral cervical vagotomy reduced the distension-evoked fall in intragastric pressure but had no effect on the corresponding fall in blood pressure. 4. Granisetron or ICS 205-930 (1-1000 micrograms kg-1, i.v.) had no effects on duodenal intraluminal pressure, but reduced the responses to distension with a bell-shaped dose-response relationship. Ondansetron (1-1000 micrograms kg-1, i.v.) did not reduce the reflex responses. 5. These results show that the 5-HT3 receptor antagonists used exerted different effects on the reflex responses to duodenal distension.

Animals↗

PubMed1989

Abnormalities of responses to autonomic stimulation in the mouse urinary bladder associated with Semliki Forest virus-induced demyelination.

The responses to autonomic stimulation of the urinary bladder were studied in mice infected with Semliki Forest Virus, which has been proposed as an animal model for multiple sclerosis. Mice infected with Semliki Forest Virus showed a decreased body weight when compared with control animals, although their bladders were proportionately heavier. The pharmacological results indicated a selective change in purinergic transmission in the bladders of mice infected with Semliki Forest Virus, while cholinergic transmission remained unchanged. This was demonstrated by a significant increase in the contractile response to beta,gamma-methylene ATP accompanied by an increase in the proportion of the nerve-mediated response blocked by alpha,beta-methylene ATP. In contrast, the contractile response to acetylcholine and the atropine-sensitive component of the neurogenic response were not significantly different between the two groups of animals. Active length-tension curves were also unchanged in the mice infected with Semliki Forest Virus when compared with controls. The results are discussed in relation to those obtained from models of urinary bladder dysfunction associated with hypertrophy; whether the alteration of atropine-resistant (purinergic) function reported here is a general secondary feature of this type of bladder dysfunction or a change specific to the Semliki Forest Virus model of multiple sclerosis is not resolved. This study provides evidence that peripheral changes as well as central nervous system demyelination occur in the Semliki Forest Virus-infected mouse.

Acetylcholine↗

PubMed1987

The seminal vesicle in eight and 16 week streptozotocin-induced diabetic rats: adrenergic, cholinergic and peptidergic innervation.

The autonomic innervation of the seminal vesicle from 8 and 16 week streptozotocin-induced diabetic rats and age-matched controls was studied by pharmacological, histochemical and immunohistochemical methods. Contractions in response to electrical field stimulation, which were abolished using prazosin (2 microM) or tetrodotoxin (one to 1.6 microM), and to noradrenaline were significantly increased in both eight and 16 week diabetic animals. The contractile response to acetylcholine was significantly increased in the 16 week diabetic rats only, when compared with controls. Although these responses were significantly increased, no difference was found in ED50 and EF50 values between control and diabetic rats. Vasoactive intestinal polypeptide (0.3 microM) had no effect on resting tension or nerve-mediated responses. In seminal vesicles from control animals, both vasoactive intestinal polypeptide-immunoreactive and acetylcholinesterase-containing nerves were localised around the folds of the columnar epithelium of secretory cells, in contrast to neuropeptide Y-immunoreactive and catecholamine-containing nerves which were found in the smooth muscle layers. In seminal vesicles from both eight and 16 week diabetic animals no difference was seen in distribution or density of acetylcholinesterase-containing nerves; there was an increase in density and fluorescence intensity of vasoactive intestinal polypeptide- and neuropeptide Y-immunoreactive nerves and a decrease in catecholamine-containing nerves compared with controls. The results are discussed in relation to autonomic neuropathy in diabetes.

Acetylcholine↗

PubMed1987

A study of bladder dysfunction during streptozotocin-induced diabetes in the rat using an in vitro whole bladder preparation.

An in vitro whole bladder preparation has been used in this study to examine the effects of eight and 16 week streptozotocin-induced diabetes on detrusor function in the rat. In eight week animals cystometric recordings showed an increase in bladder capacity associated with a decrease in intraluminal pressure. Concentration-response curves revealed a significant increase in sensitivity of the detrusor to beta,gamma-methylene ATP, a potent purinergic agonist, and a trend towards subsensitivity to acetylcholine in bladders from eight week diabetic rats when compared to controls. The atropine-resistant (purinergic) response to neurogenic stimulation was increased over the frequency range two to 30 Hz and was significantly greater at two Hz. In 16 week animals the cystometrogram had partially recovered; capacity had decreased compared to eight week diabetics and intraluminal pressure was within the normal range. Concentration-response curves revealed no significant difference in the response to acetylcholine and a greatly reduced response to beta,gamma-methylene ATP in the 16 week diabetics compared to controls. The atropine-resistant neurogenic response was slightly, but not significantly reduced. The results are discussed in relation to clinical urodynamic measurements of human detrusor dysfunction in diabetes.

Acetylcholine↗

PubMed1986

Ethylcholine mustard aziridinium ion (AF64A) impairs cholinergic neuromuscular transmission in the guinea-pig ileum and urinary bladder, and cholinergic neuromodulation in the enteric nervous system of the guinea-pig distal colon.

AF64A was examined for its ability to impair cholinergic neurotransmission in the autonomic nervous system. In the guinea-pig ileum AF64A impaired cholinergic neuromuscular transmission. In the guinea-pig urinary bladder AF64A selectivity impaired the cholinergic but not the purinergic component of neuromuscular transmission. In the guinea-pig colon circular muscle AF64A impaired cholinergic neuromodulation of the inhibitory transmission but not the inhibitory transmission itself. The nature of impairment of cholinergic transmission by AF64A is discussed.

Acetylcholine↗

PubMed1985

A comparative study of electrical field stimulation of the guinea-pig, ferret and marmoset urinary bladder.

The spontaneous and electrically evoked activity was examined in guinea-pig, ferret and marmoset urinary bladder. Electrical field stimulation of detrusor strips in vitro induced a rapid, frequency-dependent contraction with a maximum response at 40 Hz. This contraction was partly decreased by either atropine (0.29 microM) or desensitisation to alpha, beta-methylene ATP (alpha, beta-MeATP) (5 microM), and was totally blocked by a combination of the two. Atropine blocked responses to carbachol (30 microM) but not to ATP (80 microM), whereas desensitisation to alpha, beta-MeATP blocked those to ATP but not to carbachol. The nature of the excitatory neurotransmission mechanism in the bladder of those species examined in the present experiments was shown to be similar to that of other species described previously.

Adenosine Triphosphate↗