Effect of PGD2, PGE2, PGF2α and PGI2 on blood pressure, heart rate and plasma catecholamine responses to spinal cord stimulation in the rat

Laboratory of Clinical Science, National Institute of Mental Health Bethesda, Maryland 20205 USA
Prostaglandins 03/1981; 21(2):189-206. DOI: 10.1016/0090-6980(81)90137-4
Source: PubMed


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 PGE2 (10-30 microgram/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. PGI2 (0.03-3.0 microgram/kg. min, i.v.) suppressed the blood pressure response to spinal cord stimulation without any effect on heart rate or the plasma catecholamine levels, PGE2 and PGF2 alpha (10-30 microgram/kg. min, i.v.) did not change the blood pressure, heart rate or plasma EPI and Ne responses to the spinal cord stimulation although PGF2 alpha disclosed an overall vasopressor effect during the pre-stimulation period. At the pre-stimulation period it was also observed that PGE2, PGF2 alpha and PGI2, had a positive chronotropic effect on the heart rate, the cardiac accelerating effect of PGE2 was not abolished by propranolol. These in vivo studies suggest that in the rat, PGE2 and PGI2 modulate sympathetic responses, primarily by interaction with the post-synaptic elements - PGE2 on both blood vessels and the heart and PGI2 by acting principally on blood vessels.

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