The initial pressor and metabolic effects of 8-OH-DPAT are mediated by the adrenal medulla, likely via adrenaline release, whereas its sustained cardiovascular effects are not.
Answers are grounded in this paper and cite their sources.
Adrenal medulla mediates acute effects of 8-OH-DPAT in rats; leaves open translation to human 5-HT1A pharmacology.
Intravenous administration of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 150 micrograms kg-1) into conscious sham-operated rats caused significant increases in basal glycaemia with minor changes in basal insulinaemia. Glucose-stimulated (intravenous glucose tolerance test) plasma insulin levels were significantly inhibited in 8-OH-DPAT-treated sham-operated animals. These metabolic changes were associated with significant and sustained falls in blood pressure (BP) and heart rate (HR) preceded by transient (less than 5 min) increases only in BP. 2. In adrenodemedullated animals, 8-OH-DPAT failed to cause an initial vasoconstriction, hyperglycaemia, or inhibition of glucose-stimulated plasma insulin despite eliciting falls in BP and HR that were comparable to those observed in sham-operated animals. 3. Noradrenaline, adrenaline and dopamine levels in the adrenal tissue were reduced by about 95% in adrenodemedullated rats as compared to sham-operated rats. A functionally intact adrenal cortex was indicated by the presence of corticosterone in the plasma of both adrenodemedullated and sham-operated rats. 4. The present data demonstrate that 8-OH-DPAT mediates an initial increase in BP and changes in metabolic parameters via intact adrenal medulla and may thus be consequential to the release of adrenaline, whereas the sustained cardiovascular effects of 8-OH-DPAT are not.
No takes yet. Share an insight, caveat, or question.
Bouhelal et al. (1992) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: