Studies on the mechanism of central cardiovascular and temperature responses to prostaglandin D2.

Administration of prostaglandin D2 (PGD2) into the left lateral cerebral ventricle (i.c.v.) of urethane anaesthetized rats caused increases in blood pressure, heart rate and body temperature. Pretreatment of the animals with the alpha-receptor blocking drug prazosin completely prevented the PGD2-induced rise in blood pressure, but did not affect the chronotropic and hyperpyrexic effects of PGD2. Pretreatment of the rats with the beta-receptor blocking drug propranolol completely suppressed the increase in heart rate, augmented the rise in blood pressure, but reduced the temperature increase by more than 50%. These data indicate that central activation of the sympathetic nervous system mediates the cardiovascular and important parts of the temperature effects of i.c.v.-injected PGD2. The peripheral vasoconstriction (due to the stimulation of sympathetic alpha-receptors) causing the blood pressure increase is obviously of minor importance for the rise in body temperature. In contrast the enhanced production of heat by several organs following beta-receptor activation seems to be an important factor for the temperature increase.