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Biomedical subjects

C Chapman

Publications and source records attributed to C Chapman.

At least 145 records · Page 8Linked to original sources
PubMed1986

Central release of oxytocin, vasopressin and neurophysin by magnocellular neurone depolarization: evidence in slices of guinea pig and rat hypothalamus.

Using slices of rat hypothalamus maintained in vitro, we have examined release of oxytocin and vasopressin under conditions of increased neuronal activity. We report here that when the supraoptic or paraventricular nucleus is depolarized with high K+ solutions, hormone is released into areas close to the nucleus. Similar experiments with guinea pig hypothalamus suggest that neurophysin may also be co-released with oxytocin and vasopressin. Use of acetylcholine to selectively stimulate vasopressin neurones appears to evoke a rise in local release of vasopressin but not oxytocin. These results suggest that under conditions of increased neuronal activity, hormones normally secreted from the neurohypophysis are secreted locally into the hypothalamus.

Acetylcholine↗
PubMed1986

Raised levels of calcium-binding protein in plasma following insulin-induced hypoglycaemia in the pig.

Insulin-induced hypoglycaemia in the pig elicited sharp increases in the plasma concentrations of vitamin D-dependent calcium-binding protein (CaBP) and cortisol and a decrease in plasma inorganic phosphate. Glucose infusion following insulin administration abolished the increases in plasma CaBP and cortisol in response to insulin and reduced the hypophosphataemia. The percentage increases in plasma CaBP and cortisol in response to insulin-induced hypoglycaemia were reduced when the pigs were fed a low-calcium diet, but the hypophosphataemic response was similar. We conclude that insulin-induced hypoglycaemia leads to increased plasma CaBP in pigs fed a normal calcium diet, which is associated with the hypoglycaemia rather than being a direct effect of insulin. We therefore suggest that plasma CaBP may represent more than a mere uncontrolled leak from its sites of storage.

Animals↗
PubMed1986

Vasopressin, but not oxytocin, is released in response to water deprivation in conscious goats.

Plasma samples obtained at 4-h intervals from goats for at least 24 h before and then during 24 h of deprivation of water were analysed by radioimmunoassay for vasopressin and oxytocin concentrations. The samples were also analysed for osmolality and sodium concentration. The differential effect of night/day versus day/night deprivation was also studied. During the two periods before the two deprivations osmolality varied in a regular manner, with low values occurring at 08.00 h. Sodium concentration followed osmolality, whereas vasopressin did not vary during the period before deprivation. During deprivation vasopressin increased along with osmolality and sodium concentration, with the beginning of the increase occurring after the morning feed. Oxytocin levels did not increase during the period of deprivation. These results do not support the hypothesis of general release of neurohypophysial hormones in response to osmotic stimuli but instead indicate there are species variations with respect to hormonal response to water deprivation.

Animals↗
PubMed1986

The acute effects of pergolide in cyclical oedema.

The acute effects of a single 10 micrograms dose of a new dopamine agonist, pergolide, were investigated in 6 healthy women and 6 women with cyclical oedema. There was a prompt and significant reduction in mean plasma prolactin concentrations with maximum suppression occurring at 4 hours in both groups. However, the prolactin suppression was significantly less in the women with cyclical oedema. This is further evidence for a prolactin disturbance in cyclical oedema, and consistent with the proposal that reduced dopaminergic tone may be an important abnormality in the disorder.

Adult↗
PubMed1985

Motor proficiency in dyslexic children with and without attentional disorders.

Motor proficiency, in terms of speed, rhythm and absence of overflow, has previously been shown to distinguish nonlearning disabled hyperactive boys from matched controls. Accepted screening methods for selecting children with dyslexia do not include assessments of hyperactivity or other attentional deficits. Dyslexic children selected in this customary manner were compared with an otherwise matched group that had been screened for attentional disorders, on a series of repetitive and alternating movements of the fingers, hands, and feet. The screened dyslexic group performed more rapidly on five of six movements and had fewer qualitative signs of dysrhythmia or overflow.

Attention Deficit Disorder with Hyperactivity↗
PubMed1985

Neurohypophysial opioids and oxytocin secretion: source of inhibitory opioids.

When electrical stimuli are applied to the neural stalk of the pituitary, oxytocin, vasopressin, and probably several opioid peptides also contained in nerve terminals in the gland are released: one action of the released opioids appears to be to inhibit oxytocin release by an action that has been likened to pre-synaptic inhibition. Thus, when Clarke et al. (1979) stimulated the neural stalk following intravenous injection of the opioid antagonist naloxone, they observed that the evoked oxytocin release was potentiated. In the present study we confirm this result and show that oxytocin release evoked by stimulation of the supraoptic nucleus is similarly potentiated by naloxone. This finding is consistent with the hypothesis that the opioid responsible for inhibition of oxytocin release coexists with either oxytocin or vasopressin. We further report that the specific delta-receptor antagonist ICI 174864 does not potentiate oxytocin release either in vivo or in vitro. Thus, it seems unlikely that the enkephalins, putative delta-receptor agonists present in neurohypophysial fibres, are the opioids responsible for the observed inhibition of oxytocin release.

Animals↗
PubMed1985

Effects of opioid agonists and antagonists on oxytocin and vasopressin release in vitro.

The rat neurohypophysis contains both opioid receptors and substantial amounts of endogenous opioid peptides. Inhibitory influences of opioids on the secretion of both oxytocin and vasopressin have been described. We have examined the effects of a range of opioid agonists and antagonists with differing relative selectivities towards opioid receptor subclasses on the secretion of oxytocin and vasopressin from the isolated neurohypophysis. Oxytocin and vasopressin release evoked by brief periods of electrical stimulation in control experiments was compared to evoked release in the presence of test compounds. Oxytocin release was depressed approximately 25% by the delta-agonist (D-Ala2, D-Leu5)-enkephalin but not affected by putative kappa-agonists or by beta-endorphin. The use of opioid antagonists revealed a strong inhibition of oxytocin secretion by endogenous opioids released during electrical stimulation. Naloxone, relatively mu-selective, enhanced oxytocin secretion by up to 90% with a half-maximal effect at approximately 10(-6) M. MR2266, a relatively kappa-selective antagonist also enhanced oxytocin secretion but displayed agonist-like activity at high concentrations. ICI 154129, a delta-selective antagonist, was without effect on oxytocin secretion. Vasopressin release was unaffected by any of the agonists tested and not potentiated by antagonists at a range of stimulation frequencies. The data do not support the suggestion of an inhibitory endogenous opioid influence over vasopressin secretion within the neurohypophysis but indicate that an endogenous opioid peptide, possibly acting via mu- or kappa rather than delta-receptors, strongly suppresses the secretion of oxytocin.

Animals↗
PubMed1984

Reproductive hormone profiles in regularly menstruating Sudanese women.

Venous blood samples were taken daily from 21 regularly menstruating Sudanese women throughout one complete menstrual cycle. FSH, LH, estradiol-17 beta and progesterone were assayed in all plasma samples and normal reference ranges were thus established. Fifteen subjects had a luteal phase of more than 12 days whilst in 3 subjects it was shorter. Two subjects were found to be hyperprolactinemic and one had an anovulatory cycle with an elevated LH. The plasma concentrations of estradiol-17 beta in the follicular phase and progesterone in the luteal phase were significantly lower in subjects with short luteal phase than in those with a luteal phase of more than 12 days. The hormonal profile of FSH, LH, estradiol-17 beta and progesterone throughout a normal menstrual cycle in regularly menstruating Sudanese women was similar to what has been reported in the literature for other ethnic groups.

Adult↗
PubMed1984

Cycle initiation in amenorrhoea; the effect of progesterone and oestrogen administration on the pulsatile release of gonadotrophins.

The modulation of pulsatile gonadotrophin release by endogenous ovarian steroids during the normal menstrual cycle may be involved in the initiation of the following menstrual cycle. The absence of this cyclical variation may, in some cases, be the cause of, or contribute to the cause of, amenorrhoea. To assess this the modulatory effect of gonadal steroid administration on the pulsatile release of gonadotrophins was studied in fourteen amenorrhoeic and four oligomenorrhoeic women. Pulsatility was assessed by samples collected at 10 min intervals during a 4 h morning period before and after treatment with either progesterone or micronized oestradiol or a sequential combination of both. Ten patients with intact positive oestrogen-gonadotrophin feedback responded to progesterone treatment by both a significant reduction in LH pulse frequency, from a mean of 4.1 to a mean of 2.1 pulses within the 4 h study period and an increase in pulse amplitude. Progesterone therapy did not affect mean LH concentrations but there was a significant reduction in mean FSH concentrations. In the eight patients with absence of positive feedback, none of the treatment regimes elicited significant changes in LH release. No definable FSH pulses were detected before or after treatment in either group. Both the changes in LH and FSH concentrations and their release observed in this study, support the concept that cycle initiation may be related to a reduced pituitary exposure to LHRH associated with elevated progesterone concentration in the luteal phase of the cycle. This selectively induces FSH synthesis and storage. Release of this stored FSH may occur as a result of failure of the corpus luteum and falling progesterone concentrations.

Adult↗
PubMed1984

Pathological mechanisms in polycystic ovary syndrome: modulation of LH pulsatility by progesterone.

The pulsatile discharge of luteinizing hormone (LH) in nine patients with polycystic ovary syndrome (PCO) and nine patients with amenorrhoea but without PCO, who exhibited LH discharge in response to oestrogen provocation, were studied by 4-h measurement of gonadotrophin pulsatility before and after a course of progesterone injections. No significant differences were found in the gonadotrophin pulsatility patterns of the two groups, although the LH/FSH ratio rose significantly in the patients without PCO after progesterone but not in the patients with PCO, suggesting an abnormality of FSH storage. The ability to discharge gonadotrophins in response to oestrogen provocation has been reported to be present in patients with greater than or equal to 3 LH pulses in a 4-h study period. This, however, was not demonstrated in five of the nine PCO patients despite the presence of 'normal' gonadotrophin pulsatility patterns.

Adult↗
PubMed1984

Reversible fatigue of stimulus-secretion coupling in the rat neurohypophysis.

Single rat neurointermediate lobes were impaled on a stimulating electrode and continuously perifused with oxygenated medium. The secretion of oxytocin and vasopressin into the medium was measured by specific radio-immunoassays. The temporal profile of vasopressin release during a 20 min period of 13 Hz stimulation was compared with that of oxytocin. The results indicate that although the rate of secretion of both oxytocin and vasopressin declines over 20 min, the extent and time course of this fatigue is different for the two hormones. This difference could not be accounted for by differences in the rate of diffusion of released hormone from the tissue which was similar to the rate of wash-out of [14C]sucrose from the extracellular space in pre-labelled glands. In separate experiments glands were exposed to a prolonged period (60-70 min) of 13 Hz stimulation interrupted by brief silent periods (30 s-2 min duration). Some recovery from the fatigue of vasopressin secretion was evident after even the shortest of these silent periods. In further experiments glands were stimulated electrically for 18, 36, 54 and 72 s at 13 Hz: the order of presentation of the periods of stimulation was randomized between experiments. The vasopressin release rate declined markedly and progressively between 18 and 72 s. In contrast, the oxytocin release rate was relatively uniform throughout 72 s of stimulation. Thus vasopressin secretion is subject to a relatively rapid and dramatic fatigue. The results support the hypothesis that the phasic discharge patterns characteristic of vasopressin secreting neurones optimize the efficiency of vasopressin release from the nerve terminals in the neurohypophysis by avoiding the fatigue of stimulus-secretion coupling that accompanies continual stimulation.

Animals↗
PubMed1983

Evidence for a hypothalamic disturbance in cyclical oedema.

Fourteen women with cyclical oedema and six healthy female controls were investigated by use of a test in which thyrotrophin releasing hormone and luteinising hormone releasing hormone were given. Significant differences in the responses of prolactin, luteinising hormone, and follicle stimulating hormone were observed in the patients. These findings suggest that there may be a hitherto unrecognised hypothalamic defect in cyclical oedema that may account for some of the previously unexplained clinical features and lead to a more rational therapeutic approach in the management of the disorder.

Adult↗