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W Robberecht

Publications and source records attributed to W Robberecht.

63 records · Page 4Linked to original sources
PubMed1992

Angiotensin II is retained in gonadotrophs of pituitary cell aggregates cultured in serum-free medium but does not mimic the effects of exogenous angiotensins and luteinizing-hormone-releasing hormone on growth hormone release.

Angiotensin II (AII)-like immunoreactivity (LIR) was detected by immunostaining in 7.5 +/- 1.1% of cells obtained by redispersion of pituitary cell aggregates from 15- to 20-day-old female rats, cultured for 5-7 days in serum-free medium supplemented with thyroid hormone and dexamethasone. Also, renin-LIR was retained in these cultures. As shown by double immunostaining of paraffin-embedded sections of the aggregates, this AII-LIR was localized only in gonadotrophs. AII-LIR was detected at least up to 5 weeks in culture. On reversed-phase, high-performance liquid chromatography (HPLC), this AII-LIR co-migrated with authentic AII. In perifused aggregate cell cultures of 15- to 20-day-old female rat pituitary maintained in serum-free medium supplemented with dexamethasone (DEX) and triiodothyronine (T3), AII stimulated GH release. AI and AIII had a similar effect. To evaluate the possible involvement of endogenous AII in the local regulation of GH release, gonadotrophs were stimulated with luteinizing hormone-releasing hormone (LHRH). LHRH displayed a transient inhibitory effect on GH release, which was followed by a rebound of GH release after withdrawal of the peptide. Treatment of aggregates with pertussis toxin reversed this inhibitory effect into a significant stimulation of GH release. In aggregates cultured in serum-supplemented medium, LHRH provoked a significant stimulation of GH release which was still followed by a post-stimulus rebound release. In hemipituitaries from 5-day-old rats, a significant stimulatory effect of LHRH on GH release was found without rebound secretion. To evaluate the possible involvement of endogenous AII in the effects of LHRH on GH release, the influence of (Sar1,Ala8)AII, a peptide AII receptor antagonist, and of DUP753, a non-peptide AII receptor blocker was tested in various in vitro conditions. The effect of LHRH on GH release in aggregates cultured either in serum-free medium supplemented with DEX and T3 or in serum-supplemented medium was not affected by (Sar1,Ala8)AII, not even after enhancing the LHRH-induced GH release by treatment of the aggregates with pertussis toxin. A hundred times lower concentration of (Sar1,Ala8)AII, however, abolished the AII-induced changes in GH release. Also DUP753 (10 microM) failed to block LHRH-induced GH release in aggregates. (Sar1,Ala8)AII also failed to block the effect of LHRH on GH release from hemipituitaries. It is concluded that LHRH has inhibitory and stimulatory effects on GH release in cultured pituitary cell aggregates.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II↗
PubMed1990

Evidence for a pertussis toxin-sensitive signalling pathway in the dual action of angiotensin II on growth hormone release in pituitary cell aggregates.

In anterior pituitary cell aggregates cultured in the presence of the glucocorticoid dexamethasone (DEX) angiotensin II (AII) had a dual effect on growth hormone (GH) release. The peptide stimulated the release in aggregates from 2-week-old rats, whereas the peptide had an inhibitory effect in cultures from adult rats. Treatment of aggregates from adult rats with pertussis toxin (PT) reversed the inhibitory effect of AII on GH release in a stimulatory effect; PT treatment of aggregates from 18- to 20-day-old rats significantly enhanced the stimulation of GH release by AII. The effect of PT was seen only when DEX was added to the culture medium. The present data suggest that the glucocorticoid-dependent stimulus-effect coupling of AII on GH release involves both a stimulatory and an inhibitory component, the latter being abolished by PT, and that the stimulatory component predominates during immature life while the inhibitory one during adult life.

Age Factors↗
PubMed1989

Myasthenic syndrome caused by direct effect of chloroquine on neuromuscular junction.

Chloroquine induced a myasthenic syndrome in a patient taking the drug for presumable reticular erythematous mucinosis. Clinical features and results of single-fiber electromyography were typical for a failure of neuromuscular transmission, while peripheral nerves and muscles were intact on clinical, biochemical, electrophysiologic, and pathologic investigation. The time course of the clinical and electrophysiologic findings during provocation with chloroquine and the absence of autoantibodies indicate that the syndrome was due to a direct effect of the drug on the neuromuscular junction. While not taking chloroquine, the patient showed a decremental response on a modified double-step nerve stimulation test and a mean consecutive difference on single-fiber electromyography that was at the upper limit of normal, indicating a subclinical impairment of neuromuscular transmission. These findings can explain the apparent rarity of the syndrome described, as a direct effect of chloroquine on the neuromuscular junction may only have clinical relevance in patients with a reduced neuromuscular safety factor.

Adult↗
PubMed1988

Painful muscle spasms complicating algodystrophy: central or peripheral disease?

A 21 year old female patient developed Südeck's atrophy of the right foot secondary to a chronic Achilles tendinitis. The condition was complicated by the occurrence of painful muscle spasms in the right leg and incontinence of urine. The spasms had characteristics of both a tonic ambulatory foot response and a spinal flexor reflex. The movements disappeared during sleep. Regional anaesthesia of the right leg made the spasms disappear both in and outside the region of anaesthesia. Backaveraging of the EEG showed the involuntary spasms to be preceded by a cortical potential similar to a readiness potential, indicating a cortical potential similar to a readiness potential, indicating a cortical component in the pathophysiology of the muscle spasms complicating Südeck's atrophy.

Adult↗
PubMed1988

Enhanced ANG II activity in anterior pituitary cell aggregates from hypertensive rats.

Pituitary cell reaggregates from 14-day-old and adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were cultured in serum-free, chemically defined medium supplemented with the thyroid hormone triiodothyronine and the glucocorticoid dexamethasone. After 1 wk in culture, aggregates were transferred into a perifusion system, and the effect of angiotensin II (ANG II) on prolactin (PRL) and growth hormone (GH) release was studied. In aggregates from adult SHR, ANG II displayed a significant and dose-dependent GH releasing activity, whereas a negligible effect or no effect was seen in aggregates from adult WKY. In contrast, no difference in the stimulation of PRL release by ANG II was found. To exclude the possibility that the enhanced GH responsiveness was secondary to longstanding hypertension, aggregates from animals in the prehypertensive stage were studied. Both the GH and PRL responses to ANG II were significantly higher in aggregates from 14-day-old SHR than in aggregates from 14-day-old WKY. These data indicate that abnormal GH and PRL responses to ANG II exist in pituitary cell aggregates from SHR long before hypertension develops. Because these differences were found in pituitary cells maintained in culture for 1 wk, they do not seem to be secondary to changes in brain regulation of pituitary function but rather are caused by factors intrinsic to the pituitary.

Angiotensin II↗
PubMed1988

Stimulation and inhibition of pituitary growth hormone release by angiotensin II in vitro.

Rat pituitary cell aggregates cultured in serum-free chemically defined medium, single cells, and hemipituitaries were used in a perifusion system to study the influence of angiotensin II (AII) on GH release. In aggregates the peptide displayed both stimulatory and inhibitory effects on GH release, depending on the hormonal conditions of the culture medium and the age of the animal. When cultured in the absence of glucocorticoid, a modest but statistically significant stimulation was seen in aggregates from immature as well as adult animals. In aggregates from 5-day-old animals, dexamethasone (DEX) strongly enhanced the GH-releasing activity of AII in a dose-dependent way; in aggregates from 14- and 25-day-old rats, the same pattern was found, although the stimulatory action was weaker than the effect in 5-day-old rats. In aggregates from adult animals, the glucocorticoid established an inhibitory effect of AII on GH release, an effect seen with both low and high concentrations of DEX. These age- and DEX-dependent effects were not found for AII stimulation of PRL release. In the presence of DEX, AII also inhibited GRF-induced GH release in aggregates from adult animals, while it was synergistic with GRF in aggregates from developing animals. The effects of AII on GH release disappeared when aggregates were redispersed into single cells. However, in these single cell preparations AII strongly stimulated PRL release. In hemipituitaries from 1-, 5-, and 14-day-old animals, AII also stimulated GH release, but no effect was seen in hemipituitaries from 25-day-old and adult animals. These data indicate that AII has dual effects on GH release depending on the developmental stage of the animal and the hormonal environment. Furthermore, since no effect of AII was seen after redispersion of aggregates into single cells, both stimulatory and inhibitory effects seem to be based on an intercellular signaling system.

Angiotensin II↗