Effect of PGD 2, PGE 2, PGF 2α and PGI 2 on blood pressure, heart rate and plasma catecholamine responses to spinal cord stimulation in the rat

Abstract

The following experiments were designed in order to examine the inter-relationships of various prostaglandins (PG's) and the adrenergic nervous system, in conjunction with blood pressure and heart rate responses, in vivo . Stimulation of the entire spinal cord (50v, 0.3–3 Hz, 1.0 msec) of the pithed rat increased blood pressure, heart rate and plasma epinephrine (EPI) and norepinephrine (NE) concentration (radioenzymatic-thin layer chromatographic assay). Infusion of PGE 2(10–30 μg/kg. min, i.v.) suppressed blood pressure and heart rate responses to spinal cord stimulation while plasma EPI (but not NE) was augmented over levels found in control animals. PGI 2 (0.03–3.0 μg/kg. min, i.v.) suppressed the blood pressure response to spinal cord stimulation without any effect on heart rate or the plasma catecholamine levels. PGE 2 and PGF 2 α (10–30 μg/kg. min, i.v.) did not change the blood pressure, heart rate or plasma EPI and NE responses to the spinal cord stimulation although PGF 2 α disclosed an overall vasopressor effect during the pre-stimulation period. At the pre-stimulation period it was also observed that PGE 2, PGF 2 α and PGI 2, had a positive chronotropic effect on the heart rate, the cardiac accelerating effect of PGE 2 was not abolished by propanolol. These in vivo studies suggest that in the rat, PGE 2 and PGI 2 modulate sympathetic responses, primarily by interaction with the post-synaptic elements — PGE 2 on both blood vessels and the heart and PGI 2 by acting principally on blood vessels.