PMID: 2991946Jun 1, 1985Paper

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

Prostaglandins, Leukotrienes, and Medicine
U FörstermannG Hertting


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.


Jan 1, 1979·Annual Review of Physiology·L S Wolfe, F Coceani
Jun 28, 1979·Psychopharmacology·R BrusJ Zabawska
Dec 1, 1979·Proceedings of the National Academy of Sciences of the United States of America·T ShimizuO Hayaishi
Mar 1, 1976·Prostaglandins·D J Rinchuse, R R Deuben
Mar 1, 1971·British Journal of Pharmacology·H A LaveryG C Scroop
Apr 1, 1982·Prostaglandins, Leukotrienes, and Medicine·A L Sirén
Nov 1, 1982·Acta Physiologica Scandinavica·A L Sirén
Oct 1, 1982·Proceedings of the National Academy of Sciences of the United States of America·R UenoO Hayaishi

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