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.

37 Reads
  • Clinical and Experimental Hypertension 01/1982; 4(8):1335-1350. DOI:10.3109/10641968209060793 · 1.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In recent years, knowledge of the biochemistry of oxygenated metabolites of arachidonic acid has greatly increased. Their biological functions in acceleration and prevention of platelet aggregation and in inflammatory and immune reactions are becoming much clearer. The therapeutic value, particularly of PGI2 as well as selective inhibitors of synthesis, is also rapidly advancing. Despite much effort, the functional importance of prostaglandins and thromboxanes in the cNS in normal ongoing physiological processes is still quite uncertain. However, when parenchymal or vascular elements are damaged or invaded by extraneural cells, the synthesis of one or the other member of the eicosanoids is greatly increased and contributes significantly to pathophysiological reactions. Thus, prevention of synthesis is likely to have increasing importance in clinical neurology, particularly in cerebrovascular diseases.
    Journal of Neurochemistry 02/1982; 38(1):1-14. DOI:10.1111/j.1471-4159.1982.tb10847.x · 4.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In rats between the ages of 4 and 12 or 14 weeks, repeated daily subcutaneous administration of arachidonate (AA) at a dose of 50 or 200 mg/kg significantly retarded the development of hypertension in spontaneously hypertensive rats (SHR) but did not alter the normal age-related increase in blood pressures (BP) of normotensive (WKY) rats. Heart rates (HR) and plasma levels of norepinephrine (NE), but not epinephrine, were lower in AA-treated SHR than in saline-treated animals. AA-treated SHR and WKY gained less weight than the saline-treated controls. In pithed AA-treated SHR, stimulation of the sympathetic outflow (50 V, for 1 minute at 0.3 or 3.0 Hz) and intravenous administration of NE (0.3 or 3.0 g/kg) evoked smaller pressor responses than in saline-treated controls, but the stimulation-evoked increases in plasma catecholamines were unchanged by AA treatment. These results indicated that, in SHR, chronic AA treatment reduces BP by mechanisms that do not directly affect NE release from sympathetic nerves. There appears to be both reduced central nervous system activation of the sympathetic outflow and diminished responses to peripheral sympathetic stimulation and exogeneous NE which may be secondary to the reduced vascular hypertrophy that usually accompanies the development of high BP in SHR.
    Hypertension 03/1983; 5(2):172-9. DOI:10.1161/01.HYP.5.2.172 · 6.48 Impact Factor
Show more