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Biomedical subjects

H Meurs

Publications and source records attributed to H Meurs.

63 records · Page 4Linked to original sources
PubMed1982

Characterization of (-)-[3H]dihydroalprenolol binding to intact and broken cell preparations of human peripheral blood lymphocytes.

In this study we compared characteristics of (-)-[3H]dihydroalprenolol ([3H]DHA) binding sites in crude membrane preparations of human peripheral blood lymphocytes with those of intact, viable cells. A valid determination of specific beta-adrenergic receptor binding in both preparations was obtained by defining non-specific [3H]DHA binding with 10(-6) M l- or dl-propranolol or 10(-3) M l-isoproterenol. Higher concentrations of propranolol were used in prior reports on lymphocyte membranes. We showed that these concentrations may inhibit non-specific binding, causing non-saturability and inhomogeneity of the estimated 'specific' binding. In the intact cell preparations, inclusion of 10(-4) M phentolamine was necessary to reduce the high degree of non-specific binding. By contrast, phentolamine (10(-4) M) showed no effect on the [3H]DHA binding to membrane preparations. At 37 degrees C the [3H]DHA binding to beta-adrenergic receptor sites in both intact and broken cell preparations was rapid and reversible. The sites were stereoselective, as l-propranolol was about two orders of magnitude more potent to inhibit [3H]DHA binding than was the d-isomer. In both preparations, agonists competed for specific binding with a rank order of potency isoproterenol greater than epinephrine greater than norepinephrine, which indicated a beta 2-type of adrenergic receptor. The specific [3H]DHA binding was saturable and Scatchard analysis revealed comparable numbers of homogeneous, non-cooperative binding sites (approximately 1250 receptors/cell in the membrane preparations and 1700 receptors/cell in the intact cells). In spite of these similarities the membrane sites showed a lower affinity for the antagonists [3H]DHA and propranolol than did the intact cell sites, whereas their affinity for the agonists was increased. These differences indicate that the membrane system might be less suited to provide physiologically significant information about the beta-adrenergic receptor system.

Alprenolol↗
PubMed1982

The beta-adrenergic system and allergic bronchial asthma: changes in lymphocyte beta-adrenergic receptor number and adenylate cyclase activity after an allergen-induced asthmatic attack.

Beta-adrenergic receptor characteristics and adenylate cyclase responses to different stimuli were measured in lymphocyte membrane preparations of six normal control subjects and five allergic asthmatic patients with mild airways disease and increased bronchial reactivity to histamine and acetylcholine. The determinations were performed just before and 24 hr after inhalation challenge with house-dust mite antigen to investigate the influence of an allergen-induced asthmatic attack on the beta-adrenergic receptor system. Before the house-dust mite challenge, the lymphocyte membranes of the patients showed a normal receptor density, dissociation constant for (-)3H-dihydroalprenolol, and adenylate cyclase response to isoproterenol, guanyl-5'-yl-imidodiphosphate, (GppNHp) and NaF. After the allergen-induced asthmatic reaction, however, the beta-adrenergic receptor number in the patients was significantly reduced by 21%, while the basal adenylate cyclase activity and isoproterenol-, GppNHp-, and NaF-induced cyclic AMP responses were simultaneously reduced by about 40%. The allergen challenge had no significant effect on the lymphocyte membranes of the control subjects. These results suggest (1) that a reduced beta-adrenergic function is not an intrinsic component of allergic bronchial asthma but is rather the consequence of an active disease state, and (2) that next to changes in beta-adrenergic receptor number, alterations distal to the receptor may play an important role in the observed decrease in beta-adrenergic responsiveness.

Adenylyl Cyclases↗
PubMed1982

Protective effect of disodium cromoglycate on propranolol challenge.

The protective activity of cromoglycate in histamine and propranolol bronchial provocation tests was studied in seven asthmatic patients by inhalation of increasing doses of histamine and propranolol in the absence and presence of inhaled cromoglycate. Cromoglycate showed a significant protective effect on the propranolol challenge, whereas no protection against histamine challenge could be observed.

Adult↗
PubMed1982

The role of the adrenergic system in allergy and bronchial hyperreactivity.

The adrenergic system may have an influence on the severity and activity of bronchial asthma. It has been suggested that there might be a relationship between the allergic process and the adrenergic system. Therefore this system was studied before and after an allergen challenge. Two parameters were measured: in vivo: propranolol threshold measurement to assess adrenergic involvement; in vitro: the beta-adrenergic response of peripheral lymphocytes as parameter for beta-receptor function. Seven allergic asthmatics who were not treated with beta-stimulants or corticosteroids and seven normals inhaled house dust mite extract. On the days before and after the challenge, propranolol threshold measurements were performed. Six patients had a dual reaction after a house dust mite inhalation; one patient had an early response. The propranolol threshold changed from 1.32% (SEM 0.16) on the day before challenge to 0.86% (SEM 0.19) on the day after (0.02 less than P less than 0.025). In the same patients the maximal cAMP response of lymphocytes in the presence of 10(-6) mM isoproterenol changed from 339% (SEM 18.9) above basal level before the allergen challenge to 194% (SEM 24.6) after the challenge (0.001 less than P less than 0.005). The pre-challenge beta-response of lymphocytes of the asthmatic patients was comparable with that of normal lymphocytes (298% SEM 59.8). The results suggest that an allergen-induced asthmatic attack may lead to an impaired beta-adrenergic function.

Adolescent↗
PubMed1979

Laboratory of Physiological Chemistry, State University Groningen, Netherlands.

To obtain more information about the arrangement of Hind III restriction fragments in the tRNA-rRNA region of the Neurospora crassa mitochondrial (mt) DNA we have cleaved the mtDNA with Hpa I and Hind II. We could construct additional cleavage maps for these enzymes. Hybridization of rRNAs to Hind II fragments confirmed the existence of an intervening region of about 2,300 basepairs in the 24S rRNA (Hahn et al., Cell, in press). About seven tRNA genes, among which the genes for tRNA1Ser and tRNAMetM, are located in a segment of about 5,000 bp separating the 24S and 17S rRNA genes. Another cluster of 14 tRNA genes is found adjacent to the other end of the 24S gene. The genes for tRNALeu1 and tRNAMetF are located in this cluster.

DNA Restriction Enzymes↗
PubMedDate not supplied

Some fundamental points concerning the clinical aspects of desensitization.

Continued exposure of target cells to a hormonal agonist frequently leads to a blunted response to that agonist. This process has been termed desensitization, refractoriness, tolerance or tachyphylaxis. The receptor involved in case of beta-sympathomimetics is the beta-adrenergic receptor. When the clinical aspects of beta-adrenergic receptor desensitization are considered, a number of points need serious attention: 1) the route of administration of the drug and the concentration of the drug reached at the receptor site; 2) other factors which may cause reduced responsiveness of the beta-adrenergic receptor besides beta-sympathomimetics and interfere with this process; 3) the different cell-types which are studied and thought to be representative for processes taking place at lung tissue level; 4) the in vivo parameter(s) chosen to describe desensitization; 5) the difference between normal and asthmatic subjects; 6) the mechanism behind desensitization. The paper concerns a review of these points. Since the clinical findings with respect to the induction of desensitization by beta-sympathomimetics are rather controversial, the therapeutic advice should be: use it with caution.

Adenylyl Cyclases↗