Central action of PGE1 on the cerebral neurotransmission; the cardiovascular response

PGE1 administered in a single dose of 27 nmol intracerebroventricularly (icv) into the rats under urethane anaesthesia caused a long-lasting increase of the blood pressure and tachycardia. Phenoxybenzamine given 60 min before (20 mg/kg ip) blocked the hypertension and tachycardia evoked by PGE1 icv administration. Moreover, reserpine (10 mg/kg ip) given 24 h before PGE1 injection caused similar effects. Previous degeneration of the central adrenergic neurons (6-hydroxydopamine, 2 x 250 micrograms icv) also reduced both exerted effects by PGE1 icv. From the experiments carried out it results that central cardiovascular effects of PGE1 are due to the intact cerebral neurotransmission. These described effects could be common with direct PGE1 action upon adrenergic receptors from indirect effects due to release of noradrenaline by PGE1 in the central nervous system (CNS) in rats.