Article date: September 1991
By: M. Portillo, M. Reverte, D. Langin, J.M. Senard, M.A. Tran, M. Berlan, J.L. Montastruc, in Volume 104, Issue 1, pages 190-194
The present study investigates the influence of a 7‐day treatment with 2 mg kg−1, s.c., twice daily of RX 821002 (an α2‐adrenoceptor antagonist which binds only to α2‐adrenoceptors) or idazoxan (α2‐antagonist which binds to α2‐adrenoceptors and also to non‐adrenoceptor idazoxan binding sites: NAIBS) on α2‐adrenoceptor (labelled with [3H]‐RX 821002) and NAIBS (labelled with [3H]‐idazoxan) number in three tissues (adipocytes, colocytes and platelets) in the rabbit.
Acute administration of RX 821002 or idazoxan increased plasma non‐esterified fatty acids (NEFA) and catecholamine levels with no change in plasma glucose levels.
The 7‐day treatment with RX 821002 or idazoxan failed to influence food intake, total body weight or perirenal adipose tissue weight.
RX 821002 and idazoxan increased the number of [3H]‐RX 821002 binding sites in adipose tissue with no change in colocytes or platelets.
RX 821002 and idazoxan failed to modify [3H]‐idazoxan binding sites on adipocytes and colocytes. No significant [3H]‐idazoxan binding was detected on rabbit platelets.
The results show that a 7‐day treatment with α2‐antagonists induces an up‐regulation in adipocyte α2‐adrenoceptors. In contrast, this phenomenon does not involve all the tissues since colocytes and platelets escape the effects of α2‐antagonists. The data suggest a differential regulation of α2‐adrenoceptors according to their location.
The fact that NAIBS did not vary suggests that α2‐adrenoceptors and NAIBS are two different entities. Finally, since RX 821002 and idazoxan exert similar effects after either acute or chronic treatment, it is suggested that NAIBS are not involved in the control of catecholamine release or in NEFA or glucose metabolism.
The present study investigates the influence of a 7‐day treatment with 2 mg kg−1, s.c., twice daily of RX 821002 (an α2‐adrenoceptor antagonist which binds only to α2‐adrenoceptors) or idazoxan (α2‐antagonist which binds to α2‐adrenoceptors and also to non‐adrenoceptor idazoxan binding sites: NAIBS) on α2‐adrenoceptor (labelled with [3H]‐RX 821002) and NAIBS (labelled with [3H]‐idazoxan) number in three tissues (adipocytes, colocytes and platelets) in the rabbit.
Acute administration of RX 821002 or idazoxan increased plasma non‐esterified fatty acids (NEFA) and catecholamine levels with no change in plasma glucose levels.
The 7‐day treatment with RX 821002 or idazoxan failed to influence food intake, total body weight or perirenal adipose tissue weight.
RX 821002 and idazoxan increased the number of [3H]‐RX 821002 binding sites in adipose tissue with no change in colocytes or platelets.
RX 821002 and idazoxan failed to modify [3H]‐idazoxan binding sites on adipocytes and colocytes. No significant [3H]‐idazoxan binding was detected on rabbit platelets.
The results show that a 7‐day treatment with α2‐antagonists induces an up‐regulation in adipocyte α2‐adrenoceptors. In contrast, this phenomenon does not involve all the tissues since colocytes and platelets escape the effects of α2‐antagonists. The data suggest a differential regulation of α2‐adrenoceptors according to their location.
The fact that NAIBS did not vary suggests that α2‐adrenoceptors and NAIBS are two different entities. Finally, since RX 821002 and idazoxan exert similar effects after either acute or chronic treatment, it is suggested that NAIBS are not involved in the control of catecholamine release or in NEFA or glucose metabolism.
DOI: 10.1111/j.1476-5381.1991.tb12406.x
View this article