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Biomedical subjects

M A Devynck

Publications and source records attributed to M A Devynck.

At least 163 records · Page 9Linked to original sources
PubMed1982

LCEC monitoring of 5-hydroxyindolic compounds in the cerebrospinal fluid of the rat related to sleep and feeding.

A new technique which allows for both the chronic withdrawal of CSF and continuous recording of EEG sleep patterns and food intake in the freely moving rat is described. Liquid chromatography with electrochemical detection (LCEC) was used for the direct assay of tryptophan metabolites in the CSF. Both 5-hydroxyindolacetic acid (5-HIAA) and 5-hydroxytryptophan (5-HTP) were easily detectable. However, serotonin (5-HT) levels were relatively low and 5-hydroxytryptophol (5-HTPhol) and N-methylserotonin (N-Me-5HT) were undetectable in several cases. The continuous monitoring of 5-HIAA and 5-HTP indicated stable values throughout the 3-hr experiments during which no food or small meals were consumed. In the rat which consumed a large meal, both 5-HIAA and 5-HTP significantly increased following that meal. This increase in metabolites may be the result of an increased availability of tryptophan to the brain as a result of the meal. Although this study is preliminary, the described technique can provide further information about the possible relationship between behavioral (sleep and/or feeding) changes and the concomitant neurochemical fluctuations.

5-Hydroxytryptophan↗
PubMed1982

Diffuse structural alterations in cell membranes of spontaneously hypertensive rats.

Plasma membranes from heart, nerve endings, and liver were compared in 3-week-old male spontaneously hypertensive rats from the Okamoto substrain (SHR) and normotensive Wistar/Kyoto control rats (WKY) [systolic blood pressure 105 +/- 4 and 95 +/- 4 mm Hg, respectively (1 mm Hg = 133 Pa)] according to two criteria: calcium binding at physiological intracellular concentrations and polarization of an embedded fluorescent probe, 1,6-diphenyl-1,3,5-hexatriene. Whatever the tissue of origin, the density of high-affinity calcium binding sites was lower in SHR than in WKY plasma membranes, and the polarization of diphenylhexatriene fluorescence was constantly higher in SHR than in WKY membranes. These membrane abnormalities are similar to those previously described in the erythrocyte membrane from SHR. The presence of diffuse structural alterations in cellular membrane from young spontaneously hypertensive rats when blood pressure is still in the normotensive range suggests a genetic origin. Such inherited abnormalities may by themselves participate in the rise in blood pressure.

Animals↗
PubMed1982

High-affinity calcium binding in rat synaptosomal plasma membranes: decrease in young, genetically hypertensive rats.

A large number (about 4--5 nmol/mg of protein) of high-affinity (apparent dissociation constant at 37 degrees C: KD37 degrees C = 5 x 10(-8) M) calcium binding sites was characterized in synaptosomal membrane fractions enriched in plasma membranes that were isolated from rat brain. These sites were studied simultaneously in membranes from spontaneously hypertensive young rats (SHR) and their normotensive controls. No difference was observed between whole synaptosomes from these two substrains. However, plasma membrane-enriched fractions from SHR exhibited a reduced calcium binding capacity without a significant change in affinity. This decrease which averaged 15--20% was not due to any variation in the accessibility of calcium to its binding sites, as similar results were obtained in the presence of the calcium ionophore A23187. The reduction found in calcium binding is very similar to that previously described in erythrocyte membranes. It is envisaged that such an abnormality at nerve endings might play a role in the pathogenesis of genetic hypertension.

Acetylcholinesterase↗
PubMed1982

Regional distribution of noradrenaline and dopamine-beta-hydroxylase in the brain of spontaneously hypertensive rats.

The catecholamine concentration and dopamine-beta-hydroxylase activity were determined in several nuclei of the brain of spontaneously hypertensive rats (SHR) compared with Wistar Kyoto (WKY) controls. Catecholamines were measured by using liquid chromatography coupled with electrochemical detection. The threshold of detection was 5 X 10(-14) mole. Dopamine-beta-hydroxylase (DBH) was assayed by a sensitive radioenzymatic assay using tyramine as the substrate. The limit of detection was 5 pmoles of octopamine per sample. Significantly lower noradrenaline content was observed in 4 week-old SHR in some medullary and hypothalamic areas which are involved in cardiovascular regulation. This abnormally was no longer detectable in 12 week-old rats. The changes in catecholamine levels observed in young rats were not observed during the development of deoxycorticosterone-salt hypertension and therefore probably do not represent a compensatory mechanism tending to limit the progressive rise blood pressure. No significant difference in DBH activity was observed between the young SHR and WKY in any brain region measured. The altered relationship between noradrenaline content and DBH activity observed in young SHR when compared to WKY suggests a change in noradrenergic neurones activity and/or structure which could correspond to a genetically transmitted neurochemical abnormality associated with the initiation of hypertension in the SHR.

Age Factors↗
PubMed1982

[Implication of anterior hypothalamic dopamine in the regulation of arterial pressure].

The anterior hypothalamus is essential for the normal carotid sinus baroreceptor reflex. The dopamine innervation to this region is a projection from the dopaminergic A 14 cell group of the rostral hypothalamus. The anterior hypothalamic/preoptic region (AH/PO) was unilaterally superfused with buffer containing L-DOPA (10(-4) M) and the superfusate analyzed for dopamine using liquid chromatography with electrochemical detection. A stable release of dopamine was analyzed for dopamine using liquid chromatography with electrochemical detection. A stable release of dopamine was obtained within one hour. When the baroreceptor reflex loop was activated, a concomitant increase in dopamine release was observed. Lesions of the ventral noradrenergic bundle by a knife cut significantly increased the release of dopamine for at least two hours. The data are compatible with a tonic noradrenergic mechanism mediating an inhibitory control of dopamine release in the AH/PO. This dopaminergic involvement may play a functional role in blood pressure control.

Animals↗
PubMed1981

In vivo dopamine release from the anterior hypothalamus of the rat.

The release of dopamine from the anterior hypothalamic/preoptic region of the anesthetized rat was investigated in vivo using a superfusion technique with a push-pull cannula. Dopamine was measured electrochemically after separation by liquid chromatography. The spontaneous release of dopamine was very low but detectable in some experiments. An inhibitor of monoamine oxidase (pargyline) and the immediate precursor of dopamine (L-DOPA) were added to synthetic cerebrospinal fluid superfusing the area. When these substances were present dopamine release was increased considerably and appeared to be stable for a long period of time. Mechanisms contributing to the formation of newly synthetized dopamine are discussed in relation to the releasing effect of d-amphetamine and the inhibiting effect of calcium-free medium. The functional significance of dopamine release was shown by the increased release of dopamine following an increase in blood pressure obtained by an intraarterial injection of blood. Finally, ventral noradrenergic bundle lesion on the same side of the superfusion site considerably enhanced dopamine release which may indicate an inhibitory control of dopamine release by noradrenergic neurons. Furthermore, this experimental procedure provides valuable means for analyzing the effects of pharmacological as well as other manipulations on the dopamine released from a superfused brain area in vivo.

Animals↗
PubMed1981

Abnormal calcium handling by isolated cardiac plasma membrane from spontaneously hypertensive rats.

1. Calcium handling by heart sarcolemmal vesicles from young spontaneously hypertensive rats (SHR) and normotensive Wistar--Kyoto (WKY) control rats were compared. 2. Calcium binding was significantly altered in SHR membranes at the physiological cytosolic Ca2+ concentrations which occur in resting and excited cells. 3. ATP-dependent calcium accumulation occurred at a higher rate in SHR than in WKY rat membrane vesicles. 4. Na+-dependent calcium extrusion of loaded vesicles was higher in SHR than in WKY rat membrane vesicles. 5. These alterations may play a significant role in the pathogenesis of hypertension.

Animals↗
PubMed1981

Distinguishing traits in the Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rats.

Distinct differences in central and peripheral noradrenaline (NA) were observed in the hypertension prone (SBH) and resistant (SBN) strain, derived from the Hebrew University SABRA rats. In the medulla oblongata NA concentration was 90% higher and tyrosine hydroxylase activity 88% lower in SBN when compared to SBH, suggesting marked strain differences in NA turnover. In this area, NA-induced cAMP generation was higher in SBH than in SBN, while the hypothalamus, the reverse situation was present. The relevance of hypertension of the reciprocal cAMP changes is still uncertain. The concentration of NA in heart tissue was significantly higher in SBN than in SBH. Doca-salt treatment caused hypertension and depletion of atrial NA in SBH, but had no effect on either blood pressure or atrial NA in SBN rats. The results suggest that resistance to hypertension in SBN rats is associated with decreased NA turnover in medulla oblongata and reduced activity of cardiac neuronal sympathetic endings.

Animals↗
PubMed1981

Calcium binding alteration in plasma membrane from various tissues of spontaneously hypertensive rat.

Calcium binding properties of plasma membrane enriched fractions from various tissues were studied in young spontaneously hypertensive rats (SHR) and their normotensive controls (WKY). In all tissues tested (heart, liver, nerve endings, erythrocytes), high affinity calcium binding sites were characterized. Their KD values were in the range of the cytosolic free calcium concentration : (10(-8)-10(-7)). Whatever the tissue, plasma membrane enriched fraction from SHR exhibited a reduced calcium binding capacity but no significant change in affinity. This decrease which averaged 15-25% was also observed in the presence of the calcium ionophore A23187 and thus does not result from a modified accessibility of calcium to its binding sites. It is suggested that this abnormality may be of genetic origin and is possibly implicated in the pathogenesis of hypertension.

Animals↗
PubMed1980

Inherited defect in a Na+, K-co-transport system in erythrocytes from essential hypertensive patients.

The Na+ and K+ electrochemical gradients across cell membranes are believed to be maintained by the action of a Na+, K+-pump. In human erythrocytes this pump exchanges internal Na+ for external K+ in approximately a 1.5 ratio. Thus, when Na+-loaded/K+-depleted erythrocytes are incubated in physiological conditions they tend to recover their original low Na+/high K+ content. Surprisingly, in erythrocytes from healthy donors the net Na+ extrusion/K+ influx ratio exceeds the 1.5 ratio predicted for Na+, K+-pump-mediated fluxes whereas it is similar to this value in erythrocytes from essential hypertensive patients and some of their descendants. We now report that this difference is due to the presence of a Na+, K+-co-transport system in normal erythrocytes which extrudes both internal Na+ and K+ and is functionally deficient in erythrocytes of essential hypertensive patients and some of their descendants. No difference in passive Na+ permeability could be detected between normotoensive and hypertensive subjects.

Binding Sites↗
PubMed1980

Early changes in noradrenaline content of some brain nuclei in spontaneously hypertensive rats.

1. The noradrenaline content of individual brain nuclei was measured by using high-pressure liquid chromatography coupled with electrochemical detection. 2. This study was performed on spontaneously hypertensive rats during the development of hypertension (4 and 12 weeks) and also on deoxycorticosterone-salt hypertensive rats after 1 and 4 weeks of treatment. 3. In young spontaneously hypertensive rats a significant decrease in noradrenaline content was observed in some medullary and hypothalamic nuclei which are involved in cardiovascular regulation. No change was observed after deoxycorticosterone-salt treatment. 4. It is proposed that a change in adrenergic activity, restricted to brain cardiovascular centres, could represent a mechanism triggering spontaneous hypertension.

Animals↗
PubMed1979

Clinical and pathological relevance of erythrocyte cation fluxes measurement in hypertension.

1. The clinical applications of a simple laboratory test for the diagnosis of essential hypertension were further investigated on a large number of patients (124 individuals). 2. The reduced erythrocyte ratio of Na+/K+ net fluxes observed in essential hypertensives might be secondary to a functional defect in a Na+-K+ cotransport system. 3. A similar reduction in the ratio of Na+/K+ net fluxes was also observed in erythrocytes of some normotensive subjects born of hypertensive parents and of genetically hypertensive rats. This suggests that the erythrocyte membrane defect follows the genetic transmission of hypertension.

Animals↗