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H Houben

Publications and source records attributed to H Houben.

13 recordsLinked to original sources
PubMed1992

Negative regulation by dexamethasone of the potentiation of neuromedin C-induced growth hormone and prolactin release by estradiol in anterior pituitary cell aggregates.

The bombesin-like peptide neuromedin C (NMC) stimulated the release of growth hormone (GH) and prolactin (PRL) from adult male rat anterior pituitary cell aggregates cultured in serum-free medium. This effect, particularly on GH release, was significantly increased when the cells were cultured in the presence of estradiol (E2). The GH response to NMC was not affected by 4 nM dexamethasone (Dex) but was enhanced in the presence of 80 nM Dex. However, the strong stimulatory action of E2 on the GH response to NMC was completely abolished by 4 nM Dex. In contrast, the PRL response to NMC was reduced by 4 nM Dex and this to a proportionally similar extent in the presence or absence of E2. The present data show that glucocorticoids can be both positive and negative regulators of the same response system.

Animals↗
PubMed1991

Evidence for the presence of gastrin-releasing peptide immunoreactivity in rat anterior pituitary corticotrophs and lactotrophs, AtT20 cells, and GH3 cells: failure to demonstrate participation in local control of hormone release.

Using antisera raised against the N-terminal (1-16) or the C-terminal part of the bombesin (BBN)-like peptide gastrin-releasing peptide (GRP) and against the C-terminus of pro-GRP, GRP- and pro-GRP-like immunoreactivity (IR) was detected by immunostaining in freshly dispersed rat anterior pituitary (AP) cells and in reaggregate AP cells cultured in serum-free medium. Depending on the antiserum used, 6.4 +/- 0.4% to 12.4 +/- 2.7% of freshly dispersed cells were immunoreactive. Solid phase preabsorption of the antisera with the respective antigens abolished the staining. GRP-IR was detectable by double immunostaining in a subpopulation of PRL cells and ACTH-containing cells. In contrast, only very few somatotrophs, gonadotrophs, and thyrotrophs were immunoreactive, and they were much smaller than the typical mature forms of these cell types. GRP- and pro-GRP-IR were also detected in the ACTH-secreting AtT20 cell line and in the PRL- and GH-secreting GH3 cell line. GRP- and pro-GRP-IR were present in AP cell aggregates maintained in culture for 4 weeks. The finding of both GRP- and pro-GRP-IR in a subpopulation of lactotrophs and corticotrophs and their persistence in culture under serum-free conditions strongly suggest that GRP-like peptides are produced in rat AP. Although the potent GRP receptor antagonist L 686,095-001C002 effectively blocks stimulation of GH and PRL release by exogenous BBN-like peptides, it failed to affect basal GH and PRL release from perifused reaggregate AP cell cultures as well as GH and/or PRL release stimulated by epinephrine, vasoactive intestinal peptide, TRH, GH-releasing factor, and angiotensin-II or PRL release inhibited by dopamine. Thus, the latter data do not support the hypothesis often suggested that peptides endogenously present in AP cells are involved in the paracrine regulation of AP hormone secretion.

Adrenocorticotropic Hormone↗
PubMed1990

Stimulation of growth hormone and prolactin release from rat pituitary cell aggregates by bombesin- and ranatensin-like peptides is potentiated by estradiol, 5 alpha-dihydrotestosterone, and dexamethasone.

The effect of the bombesin-like peptides, gastrin-releasing peptide (GRP) and neuromedin-C (NMC), and the ranatensin-like peptides, neuromedin-B (NMB), neuromedin-B30 (NMB30), and neuromedin-B32 (NMB32), on pituitary GH and PRL release was studied in perifused anterior pituitary aggregate cell cultures from 9- to 12-week-old male rats cultured in serum-free defined medium supplemented with 0.05 nM T3 and 4 nM dexamethasone (DEX). All peptides stimulated PRL and GH release. GRP and NMC stimulated hormone release in a concentration-dependent manner between 0.1-10 nM. NMB was slightly more potent than NMB30 and NMB32, but was significantly less potent than GRP and NMC. The magnitude of the PRL response to GRP and NMC inversely correlated with that of the GH response. Cultures with relatively low PRL response levels displayed high GH responses, whereas the opposite was found in cultures with high PRL response levels. The stimulatory actions of GRP, NMC, and NMB were blocked by the bombesin receptor antagonist Leu13 psi (CH2NH) Leu14-bombesin, supporting the specificity of the findings. Addition of 1 nM estradiol (E2) to the culture medium provoked an impressive (4- to 10-fold) increase in the magnitude of the GH response to NMC without changing the EC50 value (0.5 nM). In contrast, E2 significantly decreased the stimulation of GH release by rat GH-releasing factor. In the E2-treated aggregates 3 nM NMC stimulated GH release to a comparable extent as 0.1 nM GRF. 5 alpha-Dihydrotesterone (10 and 100 nM) and DEX (80 nM) also enhanced the GH response to NMC, but to a much smaller extent than E2. E2 had also a stimulatory effect on the PRL response to NMC, particularly in cultures with a low intrinsic PRL response. The PRL response to NMC was decreased by DEX and slightly augmented by 5 alpha-dihydrotestosterone. It is concluded that bombesin- and ranatensin-like peptides have a stimulatory effect on GH and PRL release at the pituitary level. Since their action on GH release is strongly potentiated by E2 and much less so by glucocorticoids, these peptides clearly distinguish their activity and specificity from that of the protagonist releasing factor GH-releasing factor, suggesting a role in sex-related differences in GH release or in the control of GH secretion during sexual maturation.

Animals↗
PubMed1988

Reproducibility of haemodynamic and plasma catecholamine responses to isometric exercise and mental arithmetic in normo- and hyper-tensive subjects.

1. To determine the reproducibility of a mental arithmetic stress test and a handgrip exercise test, we studied the responses of blood pressure, heart rate, forearm blood flow and plasma catecholamines on two occasions, with an interval of at least 1 week, in 24 normotensive and 22 hypertensive subjects. 2. The SE of a single observation of the percentage changes of blood pressure ranged from 3.9 to 9.3% in normotensive subjects and from 3.9 to 7.4% in hypertensive subjects in both tests. For heart rate, these values were 4.9-12.3% in the normotensive subjects and 4.8-5.7% in the hypertensive subjects. However, there was a wide individual scatter of these haemodynamic responses during both tests. The forearm blood flow, only measured during mental arithmetic, had an SE of a single observation of 33.7%. 3. In 10 normotensive subjects the SE of a single observation of the change in plasma noradrenaline was 0.16 nmol/l during handgrip exercise and 0.09 nmol/l during mental arithmetic. The corresponding values for plasma adrenaline were 0.04 and 0.05 nmol/l. 4. In conclusion, although both tests showed a rather low SE of a single observation for the blood pressure and heart rate responses in normo- and hyper-tensive subjects, there was a considerable individual variability. If related to the mean forearm blood flow responses, the SE of a single observation of the forearm blood flow response was of similar magnitude. The limited intra-individual reproducibility of both tests should be borne in mind when interpreting pharmacological intervention studies or studies evaluating sympathoadrenal reactivity in cardiovascular disorders.

Adolescent↗
PubMed1985

Scl-86, a marker antigen for diffuse scleroderma.

More than 300 sera from patients with a connective tissue disease were analyzed with the immunoblotting technique. The presence of autoantibodies against an 86,000-mol wt marker antigen for diffuse scleroderma (Scl-86) was found in 14 out of 33 patients with scleroderma. The presence of anti-Scl-86 antibodies seemed to correlate with the diagnosis of diffuse scleroderma since they were found in 13 out of 22 diffuse scleroderma patients and in only one out of 11 patients with limited scleroderma. All scleroderma sera (33 patients' sera and 13 reference sera) were also tested for the presence of anti-Scl-70 antibodies. It was found that all anti-Scl-70 positive sera (n = 25) contained anti-Scl-86 antibody as well, suggesting a relationship between these two antigens. However, the Scl-86 antigen was shown to be an extremely insoluble nonchromosomal protein, resistant to boiling in sodium dodecyl sulfate. This contrasts with the Scl-70 antigen, which has been described as a thermolabile, soluble antigen present in the chromatin fraction. Together, our results are consistent with the idea that Scl-70 is a degradation product of Scl-86. The Scl-86 antigen is present in freshly prepared rabbit thymus, spleen, and liver nuclei as well as in nuclei from various cultured cell lines, but is not detectable in extractable nuclear antigen from rabbit thymus. In a limited retrospective study, the anti-Scl-86 antibodies were found in two sera from patients with Raynaud's phenomenon before the development of diffuse scleroderma. Therefore, it is possible that screening of patients' serum for this antibody might predict the development of diffuse scleroderma.

Animals↗
PubMed1983

Hemodynamic and humoral effects of coffee after beta 1-selective and nonselective beta-blockade.

Several studies report a substantial rise in plasma catecholamines after caffeine. Epinephrine infusion induces a pressor response after nonselective beta-blockade. We studied the hemodynamic and humoral effects of drinking coffee after placebo and after both nonselective (propranolol) and beta 1-selective (metoprolol) blockade in 12 normotensive subjects. After placebo, coffee induced a rise in systolic and diastolic blood pressure and a fall in heart rate, whereas forearm blood flow did not change. Plasma catecholamines, especially epinephrine (+150%), rose and plasma renin activity, fell after drinking coffee. The effects of coffee on blood pressure, forearm blood flow, and all humoral parameters were not altered by pretreatment with propranolol or metoprolol. The fall in heart rate after coffee, however, seemed to be greater during propranolol. We conclude that the rise in plasma epinephrine after coffee was too small to reveal differences in reaction in propranolol- and metoprolol-pretreated subjects.

Adolescent↗
PubMed1982

Effect of low-dose epinephrine infusion on hemodynamics after selective and nonselective beta-blockade in hypertension.

We studied hemodynamic effects of low doses of epinephrine in five hypertensive patients receiving long-term treatment with propranolol and metoprolol. Epinephrine was infused at graded rates of 0.5, 1.0, 2.0, and 4.0 micrograms/min. During propranolol treatment epinephrine induced a marked pressor effect at all rates. There was a considerable rise in systolic as well as in diastolic blood pressure and heart rate fell. During metoprolol treatment there was only a slight rise in blood pressure and heart rate rose. Forearm blood flow was decreased by epinephrine during propranolol. Calculated forearm vascular resistance showed opposite effects. We conclude that infusion of small doses of epinephrine results in a marked difference in reaction in propranolol- and metoprolol-treated patients and that this may have relevance in the choice of beta blocker to be used in the treatment of hypertension.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non-selective beta-adrenoceptor blockade.

Haemodynamic effects of a cold pressor test (foot immersion for 6 min in water at 5 degrees C) without medication and after the non-selective beta-adrenoceptor blocker propranolol and the selective beta-adrenoceptor blocker metoprolol were studied in 17 volunteers. In the control study as well as in the study with the beta-adrenoceptor blockers cold exposure caused comparable changes, namely a blood pressure rise and a reduction of forearm blood flow. The increase in heart rate during cold exposure was clearly and equally reduced by both beta-adrenoceptor blockers. Plasma noradrenaline rose significantly by 47%, plasma adrenaline did not change. It is concluded, that as to this kind of stress, beta 1-selective-adrenoceptor blockade confers no important advantage over non-selective beta-adrenoceptor blockade.

Adolescent↗
PubMed1981

Haemodynamic effects of cigarette smoking during chronic selective and non-selective beta-adrenoceptor blockade in patients with hypertension.

1 Haemodynamic effects of cigarette smoking before and during chronic treatment with propranolol and metoprolol were studied in 16 patients with essential hypertension. 2 Smoking of cigarettes induced an increase in blood pressure of the same degree in all experimental sessions. Heart rate increased by 16 beats/min during smoking alone, but increased significantly less, when a beta-adrenoceptor blocker was used. Forearm blood flow decreased during smoking in both medication periods. 3 Plasma adrenaline rose significantly during smoking from 0.37 nmol/l to 0.77 nmol/l; plasma noradrenaline did not change. 4 It is concluded that the blood pressure changes induced by smoking are not essentially altered during chronic treatment with selective or non-selective beta-adrenoceptor blockade. Only the increase in heart rate is significantly less pronounced during treatment with both drugs.

Adolescent↗
PubMed1979

Influence of selective and non-selective beta-adrenoreceptor blockade on the haemodynamic effect of adrenaline during combined antihypertensive drug therapy.

1. Haemodynamic effects of adrenaline were studied in 27 hypertensive patients, succesively during treatment with propranol and metoprolol. In 12 patients beta-adrenoreceptor blockade was combined with diuretics and in 15 patients the blockade was combined with vasodilators. 2. During propranolol adrenaline caused a marked pressor effect: there was a considerable rise in systolic as well as in diastolic blood pressure and a marked fall in heart rate. During metoprolol there was only a slight rise in blood pressure and an increase in heart rate. 3. Forearm blood flow was decreased by adrenaline during propranolol and was increased during metoprolol. Calculated vascular resistance showed opposite changes. 4. Results were essentially the same when beta-adrenoreceptor blockade was combined with diuretics or with vasodilators and did not differ from previous results obtained in patients treated by blockade alone. 5. If adrenaline infusion can be considered as a model for acute stress, our results seem to favour a selective beta 1-adrenoreceptor blocking agent over a non-selective one, even when the blocker is combined with a diuretic or a vasodilator.

Adult↗
PubMedDate not supplied

Effect of the bombesin receptor blockers [Leu13, psi CH2NH-Leu14]bombesin and N-pivaloyl GRP(20-25) alkylamide (L 686,095-001C002) on basal and neuromedin C-stimulated PRL and GH release in pituitary cell aggregates.

Perifusion of rat anterior pituitary cell aggregates, cultured in estrogen-supplemented serum-free medium with 1 nM of the bombesin (BBN)-like peptide, neuromedin C (NMC), significantly stimulates GH and PRL release. This effect is dose-dependently inhibited by the BBN receptor blocker L 686,095-001C002 [an N-pivaloyl-gastrin-releasing-peptide(20-25) alkylamide]. The IC50 was 0.20 nM in the case of the GH response and 0.16 nM in the case of the PRL response. The antagonist has no effect on basal PRL or GH release. [Leu13, psi CH2NH-Leu14]BBN (psi BBN) displays an IC50 of 0.41 microM for inhibiting the GH response and 0.36 microM for inhibiting the PRL response to NMC. At a concentration of 0.5 microM or 5 microM, however, the latter antagonist stimulates PRL and GH release when perifused alone. This stimulatory effect is dose dependent, augments when aggregates are cultured in 1 nM E2 (as is the case for NMC) and is abolished by 2 nM L 686,095-001C002. It is concluded that L 686,095-001C002 is a potent and pure antagonist of pituitary BBN receptors mediating PRL and GH release, whereas psi BBN is a relatively weak antagonist with considerable partial agonist activity.

Amides↗