Action of prostaglandin synthetase inhibitors on rostral hypothalamic neurones: thermoregulation and biogenic amines

1976 ◽  
Vol 54 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Ralph M. Jell ◽  
Paul Sweatman
Keyword(s):  
Biogenic Amines ◽  
Neuronal Excitability ◽  
Prostaglandin Synthesis ◽  
Prostaglandin Synthetase ◽  
Depressant Action ◽  
Rostral Hypothalamus ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Induced Changes

Sensitivity of neurones in the rostral hypothalamus of methoxyflurane anesthetized cats to the prostaglandin synthetase inhibitors (PGSIs), salicylate and fenoprofen, has been examined using the technique of microiontophoresis. Results were compared with sensitivity to prostaglandin (PG) E1 and no noradrenaline (NA) and 5-hydroxytryptamine (5HT). Simultaneous applications of PGSIs and NA or 5HT were made to investigate the role of PG in monoamine induced changes in neuronal excitability. PGSIs did not excite these cells, but depressions were common, particularly with fenoprofen. PGE1 did not reverse the depressions. NA and 5HT responses were generally unaffected by simultaneous PGSI application and responsiveness to PGSIs was found to be unrelated to amine sensitivity.The results support the conclusion that PGSIs have a depressant action on neurones in this region, which may not be related to inhibition of prostaglandin synthesis, and that the actions of microiontophoretically applied NA and 5HT are not dependent upon PG.

Prostanoids promote pial arteriolar dilation and mask constriction to oxytocin in piglets

1993 ◽  
Vol 264 (4) ◽  
pp. H1023-H1027
Author(s):  
D. W. Busija ◽  
I. Khreis ◽  
J. Chen
Keyword(s):  
Cerebrospinal Fluid ◽  
Intravital Microscopy ◽  
Prostaglandin Synthesis ◽  
Pial Arterioles ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Csf Levels ◽  
Low Levels ◽  
Arteriolar Diameter ◽  
Baseline Diameter

We determined effects of oxytocin on piglet pial arterioles and the role of prostanoids in mediating arteriolar responses. Anesthetized piglets were equipped with closed cranial windows, and arteriolar diameter was measured using intravital microscopy. Pial arterioles were exposed to 10(-10) to 10(-4) M oxytocin. Cerebrospinal fluid (CSF) levels of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were determined using radioimmunoassay. Baseline diameter was 110 +/- 4 microns and increased to 120 +/- 6 microns at 10(-8) M (9 +/- 3%, n = 20). CSF levels of PGE2 were 697 pg/ml during baseline and increased to 1,685 +/- 316 pg/ml during 10(-6) M, 2,243 +/- 327 pg/ml during 10(-5) M, and 2,941 +/- 500 pg/ml during 10(-4) (n = 6). CSF levels of 6-keto-PGF1 alpha were 354 +/- 73 pg/ml during baseline and increased to 734 +/- 168 pg/ml at 10(-5) M and to 836 +/- 167 pg/ml at 10(-4) M (n = 5). After inhibition of prostaglandin synthesis by indomethacin (5 mg/kg i.v.), oxytocin constricted at all doses, starting at 10(-10) M (5 +/- 2%) and continuing to constrict at 10(-4) M (24 +/- 2%, n = 14). We conclude that: 1) piglet pial arterioles respond to relatively low levels of oxytocin, 2) local presence and/or production of prostanoids promotes dilation, and 3) endogenous prostanoids prevent constriction of pial arterioles to oxytocin. Our results suggest that oxytocin could play a role in the regulation of cerebral hemodynamics.

Effects of histidine on vasopressin action: role of decreased prostaglandin production

1988 ◽  
Vol 255 (4) ◽  
pp. F685-F689
Author(s):  
C. P. Carvounis ◽  
E. T. Schroeder ◽  
P. Cushley ◽  
P. Hueber ◽  
D. Patchin
Keyword(s):  
Prostaglandin E2 ◽  
Water Movement ◽  
Imidazole Ring ◽  
Prostaglandin Synthesis ◽  
Pge2 Production ◽  
Toad Bladder ◽  
Prostaglandin Production ◽  
Luminal Membrane ◽  
Inhibition Of Prostaglandin Synthesis

Addition of histidine to the serosal bath of the toad bladder increases the hydrosmotic response of vasopressin in this tissue. Because this represents primarily the effect of the imidazole ring of histidine, which is a known inhibitor of the production of prostaglandins, we evaluated whether histidine increases the response to vasopressin through decreased prostaglandin production. Histidine increases the response to vasopressin much more than 10(-5) M naproxen, even though the latter was equipotent to histidine in reducing prostaglandin E2 (PGE2) production. Furthermore, histidine was additive to naproxen in increasing the hydrosmotic effect of vasopressin, without causing a further decrease in PGE2 production. These findings suggest that histidine has an effect over and above that due to inhibition of prostaglandin synthesis. Our results suggest that histidine enhances the permeability of the tissue beneath the luminal membrane, an effect not found with naproxen. We propose that histidine increases the hydrosmotic response to vasopressin through at least two distinct mechanisms: 1) it decreases prostaglandin synthesis and thus increases luminal permeability; 2) it decreases the resistance to water movement of the tissues beneath the luminal membrane.

Role of prostaglandins in pial arteriolar response to CO2 and hypoxia

1980 ◽  
Vol 238 (2) ◽  
pp. H226-H230 ◽  
Author(s):  
E. P. Wei ◽  
E. F. Ellis ◽  
H. A. Kontos
Keyword(s):  
Arachidonic Acid ◽  
Parietal Cortex ◽  
Topical Application ◽  
Prostaglandin Synthesis ◽  
Vascular Responses ◽  
Cranial Window ◽  
Vasoconstrictor Response ◽  
Endogenous Prostaglandins ◽  
Inhibition Of Prostaglandin Synthesis

The effect of inhibition of prostaglandin synthesis on the pial arteriolar responses to arterial hypercapnia, hypocapnia, and hypoxia was studied in anesthetized cats equipped with a cranial window for the observation of the pial microcirculation of the parietal cortex. Inhibition of prostaglandin synthesis was achieved by intravenous administration of indomethacin (3 mg/kg) or AHR-5850 (2-amino-3-benzoylbenzeneacetic acid, 50 mg/kg). It was shown that the administration of these agents inhibited substantially the vasodilation in response to topical application of arachidonic acid (100--200 micrograms/ml). Inhibition of prostaglandin synthesis did not modify significantly the vasodilator responses to arterial hypercapnia or arterial hypoxia, nor the vasoconstrictor response to arterial hypocapnia. We conclude that endogenous prostaglandins are not mediators of these vascular responses in the pial microcirculation.

Effect of Inhibition of Prostaglandin Synthesis on the Natriuresis Induced by Saline Infusion in Man

1978 ◽  
Vol 54 (1) ◽  
pp. 47-50 ◽  
Author(s):  
Th. Mountokalakis ◽  
Th. Karambasis ◽  
D. Mayopoulousymvoulidou ◽  
G. Merikas
Keyword(s):  
Free Water ◽  
Prostaglandin Synthesis ◽  
Saline Infusion ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Prostaglandin Synthetase ◽  
Water Reabsorption ◽  
Post Infusion ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Natriuretic Effect

1. The effect of oral administration of an inhibitor of prostaglandin synthetase, indomethacin, on the natriuresis induced by the infusion of sodium chloride (saline) was studied in 11 healthy volunteers. 2. The administration of indomethacin did not alter sodium excretion before saline infusion, but it resulted in a significant increase of the natriuresis after saline infusion. This increase was not accompanied by any change in post-infusion urine flow rate or free water reabsorption. 3. It is suggested that intrarenal prostaglandins might suppress the natriuretic effect of saline infusion, probably by increasing sodium reabsorption in the distal nephron.

Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog

1979 ◽  
Vol 237 (3) ◽  
pp. F182-F187
Author(s):  
M. C. Blasingham ◽  
A. Nasjletti
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin Synthetase ◽  
Renal Functions ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.

Investigation of the role of prostaglandins in nitroglycerin-induced relaxation of isolated rabbit blood vessels

1983 ◽  
Vol 61 (6) ◽  
pp. 554-560 ◽  
Author(s):  
Brian M. Bennett ◽  
Joyce A. Moffat ◽  
Paul W. Armstrong ◽  
Gerald S. Marks
Keyword(s):  
Effective Dose ◽  
Blood Vessels ◽  
Prostaglandin Synthesis ◽  
Mesenteric Arteries ◽  
Krebs Solution ◽  
Rabbit Blood ◽  
Inhibit Prostaglandin Synthesis ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

The effect of inhibition of prostaglandin synthesis on nitroglycerin-induced relaxation was examined in isolated rabbit mesenteric and celiac arterial rings. An indomethacin dose of 5 μM was selected as adequate to inhibit prostaglandin synthesis as this dose prevented relaxation of the arterial rings by sodium arachidonate (3.3 μM) and by bradykinin, a peptide thought to induce vasodilation via stimulation of prostaglandin synthesis. Following 20 min pretreatment with indomethacin (5 μM), indomethacin solvent, or Krebs solution (control), the arterial rings were contracted submaximally with phenylephrine (0.5–10 μM). The degree of inhibition of phenylephrine-induced tone produced after cumulative additions of nitroglycerin (10−10 – 5 × 10−7 M) was assessed. In control celiac and mesenteric rings the responses to nitroglycerin were as follows: mean effective dose (ED50), 5.6 × 109 ± 4.5 × 10−9 M (SD) and 1.1 × 10−8 ± 5 × 10−9 M (SD), respectively; maximum relaxation, 97 ± 3% (SD) and 93 ± 7% (SD), respectively. Neither indomethacin nor indomethacin solvent affected the ED50 or maximum relaxation with nitroglycerin. We conclude that nitroglycerin-induced relaxation of rabbit celiac and mesenteric arteries appears to be mediated through a mechanism other than stimulation of prostaglandin synthesis.

Induction of water diuresis by endothelin in rats

1992 ◽  
Vol 263 (3) ◽  
pp. F516-F526 ◽  
Author(s):  
J. Schnermann ◽  
J. N. Lorenz ◽  
J. P. Briggs ◽  
J. A. Keiser
Keyword(s):  
Produced Water ◽  
Enzyme Inhibitor ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Water Diuresis ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Vasopressin Secretion ◽  
Induced Changes

Experiments were performed in anesthetized rats to examine the possibility that endothelin (ET) modifies renal epithelial function in addition to its well-established hemodynamic actions. Infusion of ET-3 at rates between 34 and 178 ng.kg-1.min-1 was in many cases followed by a rise in urine flow and a persistent decrease in urine osmolality, whereas glomerular filtration rate (GFR) did not significantly change. The extent of ET-induced diuresis was dependent on the response of GFR: in rats in which ET-3 infusion caused a marked reduction of GFR (greater than 70%) ET-induced diuresis was not seen, even though urine osmolality still fell significantly. From animal to animal, ET-induced changes of urine flow or GFR did not correlate significantly with the rate of ET-3 infusion. ET-1, another ET isopeptide, also produced water diuresis when administered in GFR-neutral doses. Urinary excretion of total solutes and of sodium was not significantly altered by ET-3. Infusion of vasopressin blunted the diuretic effect of ET-3, whereas ET-3-induced water diuresis was not measurably altered by chronic or acute treatment with a converting enzyme inhibitor or by acute inhibition of prostaglandin synthesis. Induction of water diuresis was not secondary to an inhibition of vasopressin secretion since it could be demonstrated in homozygous Brattleboro rats in which antidiuresis was produced by the infusion of vasopressin at a rate of 200 microU.kg-1.min-1. These data suggest that ET may be an inhibitory modulator of the hydrosmotic action of vasopressin at the level of the renal collecting duct.

Prostaglandin-dependent polyuria in hypercalcemia

1981 ◽  
Vol 241 (3) ◽  
pp. F224-F230 ◽  
Author(s):  
E. R. Serros ◽  
M. A. Kirschenbaum
Keyword(s):  
Flow Rate ◽  
Plasma Osmolality ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Prostaglandin E ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Final Group ◽  
Thirst Mechanism

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.

Digital x-ray mapping of nanometer-size supported bimetallic catalysts

1988 ◽  
Vol 46 ◽  
pp. 530-531
Author(s):  
L. T. Germinario
Keyword(s):  
Background Radiation ◽  
Metal Cluster ◽  
Single Element ◽  
Beam Diameter ◽  
X Rays ◽  
X Ray ◽  
Major Interest ◽  
Induced Changes

Understanding the role of metal cluster composition in determining catalytic selectivity and activity is of major interest in heterogeneous catalysis. The electron microscope is well established as a powerful tool for ultrastructural and compositional characterization of support and catalyst. Because the spatial resolution of x-ray microanalysis is defined by the smallest beam diameter into which the required number of electrons can be focused, the dedicated STEM with FEG is the instrument of choice. The main sources of errors in energy dispersive x-ray analysis (EDS) are: (1) beam-induced changes in specimen composition, (2) specimen drift, (3) instrumental factors which produce background radiation, and (4) basic statistical limitations which result in the detection of a finite number of x-ray photons. Digital beam techniques have been described for supported single-element metal clusters with spatial resolutions of about 10 nm. However, the detection of spurious characteristic x-rays away from catalyst particles produced images requiring several image processing steps.

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