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Biomedical subjects

L Diop

Publications and source records attributed to L Diop.

At least 37 records · Page 2Linked to original sources

Selective modification of renal alpha 2-adrenergic receptors in Milan hypertensive rat strain.

Cerebral and renal alpha-adrenergic receptors play an important role in the control of blood pressure. We studied alpha-adrenergic receptors in the cerebral and renal cortex of Milan hypertensive strain (MHS) and normotensive strain (MNS) rats, a genetic model of spontaneous hypertension linked to a kidney abnormality. Binding of the selective alpha 1-adrenergic antagonist [3H]prazosin and the alpha 2-adrenergic antagonist [3H]rauwolscine was used for receptor studies in tissues of prehypertensive (24-day-old) and hypertensive (60-day-old) rats. In the cerebral cortex, no between-strain differences in alpha 1-adrenergic and alpha 2-adrenergic receptor density and affinity were observed in prehypertensive and hypertensive periods. The density of these receptors increased similarly with age in MHS and MNS rats. In the renal cortex, the differences between MHS and MNS rats concerned alpha 2-adrenergic receptors only. Compared with their age-matched normotensive controls, MHS rats showed 1) a lower affinity for the antagonist (p less than 0.05) in the prehypertensive period, 2) absence of the normal age-related increase in receptor density, and 3) a lower density of [3H]rauwolscine binding sites (p less than 0.001) in the hypertensive period. In this period, studies of competitive inhibition of [3H]rauwolscine binding showed that l-epinephrine bound to one class of sites in MHS rats (pseudo-Hill plot, 0.90) and to two classes in MNS rats (pseudo-Hill plot, 0.68). In addition, the lack of any guanylylimidodiphosphate effect on the l-epinephrine competition curve observed in MHS rats suggests the uncoupling of these receptors from the guanosine 5'-triphosphate binding protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Changes in central alpha-adrenoceptors and noradrenaline content after high sodium intake in Sabra salt-sensitive and salt-resistant rats.

Several studies have suggested a correlation between sodium accumulation and the development of hypertension. However, the mechanisms whereby sodium is able to increase blood pressure remain unclear. In the present study, alpha-adrenoceptors and noradrenaline contents have been studied in the cerebral cortex, hypothalamus and medulla oblongata in the Sabra rat strain in order to define their role in the resistance or sensitivity to sodium-induced hypertension. Alpha-Adrenoceptors were defined using the selective ligands 3H-prazosin and 3H-rauwolscine for alpha 1- and alpha 2-adrenoceptors, respectively. Under normal sodium diet, alpha 2-adrenoceptor density was higher in cerebral cortex and lower in hypothalamus and medulla oblongata of SBN (salt-resistant) compared to SBH (salt-sensitive) rats. Five weeks of high sodium intake induced a decrease in alpha 2-adrenoceptor density in cerebral cortex and an increase in hypothalamus only in SBN rats. These changes abolished the differences between SBH and SBN rats observed with a normal sodium diet. No changes in density and affinity of alpha 2-adrenoceptors were observed in medulla oblongata of SBN and SBH rats. Density and affinity of alpha 1-adrenoceptors were similar in SBN and SBH rats in all the tissues studied and they were unaffected by the high sodium diet. Noradrenaline contents in cerebral cortex, hypothalamus and medulla oblongata were also similar in the two rat substrains under normal sodium diet, but high sodium intake induced a decrease cerebrocortical noradrenaline content only in SBN rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Sabra rats as a model to differentiate between Na+ and GTP regulation of alpha 2-adrenoceptor densities.

Sodium ions and guanyl nucleotides play an important role in increasing alpha 2-adrenoceptor densities in cerebral and renal cortex of normotensive rats. The in vitro effect of Na+ and GTP was investigated on cerebral and renal alpha-adrenoceptors in hypertensive (SBH, salt-sensitive) and normotensive (SBN, salt-resistant) Sabra rats. In SBH and SBN rats, guanyl nucleotides increased cerebral and renal high-affinity alpha 2-adrenoceptor densities. Sodium ions, in contrast, markedly increased cerebral and renal high affinity alpha 2-adrenoceptor densities only in SBH rats. Under these conditions, alpha 1-adrenoceptor densities were unchanged. Thus, although Na+ and GTP both increase alpha 2-adrenoceptor densities, these agents appear to mediate their regulatory effects via different membrane components. Moreover, the absence of sodium regulation of alpha 2-adrenoceptors in SBN rats may be responsible for the resistance to salt-induced hypertension.

Animals↗

Cerebral and renal alpha-adrenoceptors in Sabra hypertensive (SBH) and normotensive (SBN) rats: effects of high-sodium diet.

The aim of the present study was to investigate the effect of high (8%) versus normal (0.2%) sodium diet on cerebral and renal alpha-adrenoceptors of Sabra hypertensive (SBH) and normotensive (SBN) rats. Cerebral alpha 2-adrenoceptor densities were higher in SBN than in SBH rats. In contrast, renal alpha 2-adrenoceptor density was higher in SBH than in SBN rats. No difference in alpha 1-adrenoceptor densities was observed between the two strains. After 2 and 5 weeks of high-sodium diet, alpha 2-adrenoceptor densities were increased in renal cortex of SBH and SBN rats. In contrast, cerebral alpha 2-adrenoceptor densities were markedly decreased in SBN but not in SBH rats. alpha 1-Adrenoceptor densities were unchanged by high salt intake. Blood pressure increased only after 5 weeks of high-sodium diet, markedly in SBH and to a lesser extent in SBN rats. The variation in alpha 2-adrenoceptor densities thus preceded the blood pressure elevation. The dietary sodium-induced increase in renal alpha 2-adrenoceptor densities observed both in SBH and SBN rats does not appear to be a genetic marker of hypertension. In contrast, the marked decrease in cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension.

Animals↗

Dietary sodium regulation of alpha 2-adrenoceptors in Sabra hypertensive (SHB) and normotensive (SBN) rats.

Cerebral and renal alpha 2-adrenoceptors, modulated in vitro by sodium ions, are implicated in the control of sympathetic activity and of sodium reabsorption, respectively. The aim of the present study was to investigate the effect of high (8%) versus normal (0.2%) sodium diet on cerebral and renal alpha-adrenoceptors of Sabra hypertensive (SBH) and normotensive (SBN) rats. After two or five weeks of high sodium diet alpha 2-adrenoceptor density was increased in the renal cortex of SHB and SBN rats. In contrast, cerebral alpha 2-adrenoceptor densities were markedly decreased in SBN but unchanged in SBH rats. Blood pressure increased only after five weeks of high sodium diet, in SBH and to a lesser extent in SBN rats. The change in alpha 2-adrenoceptor densities thus preceded the blood pressure elevation. The dietary sodium-induced increase in renal alpha 2-adrenoceptor densities which precedes the blood pressure elevation does not appear to be a genetic marker of hypertension. Conversely, the marked decrease of cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension.

Animals↗

[Biochemical characterization of central alpha-adrenergic receptors].

Successively are learned in this paper general characteristics of cental alpha-adrenergic receptors and individualization of alpha 1- and alpha 2-adrenergic sub-groups, biochemical factors which are able to affect fixation of their respective ligands and finally physiological and pathological variations of alpha 1- and alpha 2-adrenergic receptors, which will allow to discuss their participation in different regulations and disorders.

Animals↗

Monoclonal antibodies to rat brain alpha-adrenoceptors.

We have developed three hybridomas that produce monoclonal antibodies to rat cerebral alpha-adrenoceptors. Splenic lymphocytes from BALB/c mice immunized with unpurified digitonin-solubilized alpha-adrenoceptors were fused with the mouse myeloma line P3-x 63-Ag 8.653 to yield hybridoma cultures producing alpha-adrenoceptor monoclonal antibodies of the IgG class. However, these antibodies inhibited both alpha 1 and alpha 2 ligand binding suggesting that some molecular homology exists between alpha 1- and alpha 2-adrenoceptors in the rat brain.

Animals↗

Specific binding of [3H]rauwolscine to alpha 2-adrenoceptors in rat cerebral cortex: comparison between crude and synaptosomal plasma membranes.

[3H]Rauwolscine, a specific, potent, radiolabelled alpha 2-antagonist, binds to distinct high- and low-affinity alpha 2-adrenoceptors in crude membrane preparations of the rat cerebral cortex. The concentration of high-affinity alpha 2-adrenoceptors was increased by addition of sodium ions or guanylnucleotides. In synaptosomal plasma membrane preparations, only the low-affinity component was found. Neither sodium or guanylnucleotides caused any increase in the concentration of these low-affinity receptors for [3H]rauwolscine.

Animals↗