Summary
The renal glycoprotein hormone erythropoietin (Epo) is the key element in the feedback
control of the production of red blood cells (RBC) in bone marrow. Excess of antidiuretic
hormone (ADH) increases the RBC mass by increasing the synthesis of Epo. The mechanism
of the Epo stimulating effect of ADH is not fully understood. Rats were treated with
ADH with or without prior injection of a Vla-receptor antagonist. Additional experiments
were carried out by stimulating the V2-receptor by desmopressin (DDAVP). Epo level
in plasma was doubled following injections of ADH. Blockade of the Vla-receptor completely
abolished the Epo stimulating effect of ADH. Neither ADH alone nor the combined giving
of Vla-antagonist and ADH had an influence on the glomerular filtration rate or the
renal plasma flow. Therefore, the increased Epo synthesis after application of ADH
cannot be explained by a constriction of renal blood vessels with consecutive ischemic
hypoxia. There is rather a direct stimulation of Epo synthesis by ADH via its receptors.
Since a selective stimulation of the V2-receptor by DDAVP did not increase to Epo
level in plasma, the observed increase of Epo is mediated by the Vla-receptor.
Key words
Rat - erythropoietin - antidiuretic hormone - VI-receptor - V2-receptor
