A vasoconstrictor cardiogenic chemoreflex induced by prostaglandin F2 alpha.

Systemic and skeletal muscle vascular responses to intracardiac prostaglandin F2 alpha (PGF2 alpha) were studied in anesthetized dogs. Resistance changes in a vascularly isolated but innervated reservoir-perfused gracilis muscle could occur only neurogenically. Injection of PGF2 alpha or serotonin (5-HT) raised systemic arterial blood pressure (BP) and caused reflex increases in gracilis muscle perfusion pressure (GMPP) that were abolished by alpha-adrenergic blockade. These changes in GMPP are opposite to the expected baroreceptor responses to an increase in BP. Subepicardial local anesthesia attenuated both delta BP and delta GMPP to 5-HT but only the delta GMPP to PGF2 alpha. Changes in BP and GMPP to 5-HT were reduced by vagotomy but not by stellate ganglionectomy. Conversely, stellate ganglionectomy significantly reduced the delta GMPP to PGF2 alpha but not the delta BP. Vagotomy affected neither delta BP nor delta GMPP following PGF2 alpha. Thus, while PGF2 alpha and 5-HT produce reflex vasoconstriction in gracilis muscle that is mediated through sympathetic efferent nerves and initiated by cardiogenic reflexes, apparently PGF2 alpha does so through sympathetic afferent and 5-HT through vagal afferent pathways. Further, since the systemic pressor response to PGF2 alpha persisted after stellatectomy, vagotomy, or local anesthesia, it is independent of the sympathetic cardiogenic chemoreflex.