Prostacyclin and prostagladin synthesis in isolated brain capillaries

Gecse, A; Ottlecz, Anna; Mezei, Zsófia; Telegdy, Gyula; Joó, Ferenc; Dux, E.; Karnushina, Irina

doi:10.1016/0090-6980(82)90074-0

Cited by 66 publications

(19 citation statements)

References 18 publications

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“…A variable amount of radiolabeled material also co-migrated with PGF2a, some of which could be 6-keto-PGEI. Assays of 9-OH PGDH activity indicated activities of [10][11][12][13] pmol/mg protein per h, further supporting this possibility. We compared PGH2 metabolism by homogenates of rabbit coronary microvessels, freshly isolated and cultured RCME cells, circumflex coronary artery, and aorta (Table II).…”

Section: Resultssupporting

confidence: 57%

“…Isolated coronary microvessels rapidly incorporated [1-'4C]AA into the phospholipid fraction, with 80-90% of the label taken up within 1 h. However, subsequent incubation of the microvessels for periods of [4][5][6][7][8][9][10][11][12][13][14] h resulted in the release of relatively (compared with the RCME cells) small amounts of labeled material comigrating with 6-keto-PGFia, PGF2,t, and PGE2. The majority of the radiolabeled material released appeared to consist of free AA and several other nonpolar compounds, probably hydroxy fatty acids (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The development of the methodology for the isolation of microvessels (i.e., <300 um in diameter, a mixture of arterioles, venules, and capillaries) from various tissues (10,11) gave investigators the ability to study the nature of AA metabolism in the microvasculature. A number of studies have described the synthesis of PGI2 by cerebral microvessels (12)(13)(14)(15)(16). However, isolated microvessels also exhibit additional pathways of prostaglandin synthesis, dependent upon the vascular bed and species examined.…”

Section: Introductionmentioning

confidence: 99%

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Arachidonic acid and prostaglandin endoperoxide metabolism in isolated rabbit and coronary microvessels and isolated and cultivated coronary microvessel endothelial cells.

Gerritsen¹,

Cheli²

1983

J. Clin. Invest.

149

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A B S T R A C T Isolated microvessels and isolated and cultured microvessel endothelial cells were prepared from rabbit cardiac muscle. Pathways of arachidonic acid metabolism were determined by measurement of exogenous substrate utilization ([1-'4C]arachidonic acid incorporation and release from intact tissue and cells;[1-'4C]prostaglandin H2 (PGH2) metabolism by broken cell preparations) and by quantification of endogenous products (immunoreactive 6-keto-prostaglandin Fla (PGFia,) and prostaglandin E (PGE) release) by selective radioimmunoassay. Rabbit coronary microvessels and derived microvascular endothelial cells (RCME cells) synthesized two major products of the cyclooxygenase pathway: 6-keto-PGFI,, (hydrolytic product of prostaglandin 12) and PGE2. A reduced glutathione requiring PGH-E isomerase was demonstrated in coronary microvessels and RCME cells, but not in rabbit circumflex coronary artery or aorta. In addition, a minor amount of a compound exhibiting similar characteristics to 6-keto-PGE, was found to be produced by microvessels and RCME cells. Measurement of endogenously released prostaglandins indicated that under basal and stimulated conditions, PGE release ex-

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Section: Resultssupporting

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Arachidonic acid and prostaglandin endoperoxide metabolism in isolated rabbit and coronary microvessels and isolated and cultivated coronary microvessel endothelial cells.

Gerritsen¹,

Cheli²

1983

J. Clin. Invest.

149

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“…Although some evidence suggests that arachidonic acid metabolites are formed primarily in cerebral vessels rather than in neuronal or glial elements, [8][9][10] there are other data that support our results. Seregi et a1.22> reported that cultured astrocytes produced large amounts of PGD2, PGE2, and PGF2a.…”

Section: Discussionsupporting

confidence: 82%

<I>Immunohistochemical Localization of Prostaglandin F<SUB>2α</SUB> in Reperfused Gerbil Brain</I>

Nakagomi

Sasaki

Ogawa

et al. 1990

Neurol. Med. Chir.(Tokyo)

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Immunohistochemical localization of prostaglandin (PG) F2a synthesized during recirculation follow ing experimental forebrain ischemia was studied in Mongolian gerbils. The bilateral carotid arteries were clamped for 5 minutes, and the brains were frozen in situ after 5 minutes of recirculation. Sham operated gerbils not subjected to arterial occlusion served as controls. Cryostat sections containing dorsal hippocampus 10,um in thickness were incubated in rabbit anti-PGF2a serum and stained with avidin-biotin-peroxidase complex after fixation in carbodi-imide and Zamboni's solution. In specimens from control animals, blood vessels were faintly stained with anti-PGF2a serum, while neurons and glial cells were less intensely stained or unstained. Specimens from reperfused gerbils demonstrated strongly positive staining for PGFZa in blood vessels, neurons (especially hippocampal pyramidal neurons), and glial cells. Staining for PGFZa in the reperfused animals was substantially di minished by pretreatment with indomethacin (10 mg/kg, i.p.). The results indicate that recirculation after forebrain ischemia results in an increase in PGFZa in neurons, glial cells, and blood vessels.

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“…The mechanism of the adaptation of the cerebral circulation to chronic NO deficiency is far less understood. Vasodilator prostanoids, released constitutively from brain microvessels (Gecse et al, 1982;Kis et al, 1999;Kövecs et al, 2001;Parfenova et al, 2002;Peri et al, 1995), are apparently involved in the maintenance of the resting cerebral blood flow in some species including humans and rats (Busija, 2002;Leffler, 1997) and enhancement of their influence may serve as a reserve regulatory mechanism in NO deficiency. We have observed a significant increase of the prostacyclin and prostaglandin E 2 levels in the cerebrospinal fluid of rats after acute NOS inhibition (Lacza et al, 2001b and unpublished observations), which may indicate the activation of a prostanoid mediated compensatory mechanism in NO deficiency.…”

Section: Introductionmentioning

confidence: 99%

Adaptation of the hypothalamic blood flow to chronic nitric oxide deficiency is independent of vasodilator prostanoids

et al. 2007

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The aim of our study was to investigate the adaptation of the hypothalamic circulation to chronic nitric oxide (NO) deficiency in rats. Hypothalamic blood flow (HBF) remained unaltered during chronic oral administration of the NO synthase (NOS) inhibitor N G -nitro-L-arginine methyl ester (L-NAME, 1 mg/ml drinking water) although acute NOS blockade by intravenous L-NAME injection (50 mg/kg) induced a dramatic HBF decrease. In chronically NOS blocked animals, however, acute L-NAME administration failed to influence the HBF. Reversal of chronic NOS blockade by intravenous L-arginine infusion evoked significant hypothalamic hyperemia suggesting the appearance of a compensatory vasodilator mechanism in the absence of NO. In order to clarify the potential involvement of vasodilator prostanoids in this adaptation, cyclooxygenase (COX) mRNA and protein levels were determined in the hypothalamus, but none of the known isoenzymes (COX-1, COX-2, COX-3) showed upregulation after chronic NOS blockade. Furthermore, levels of vasodilator prostanoid (PGI 2 , PGE 2 and PGD 2 ) metabolites were also not elevated. Interestingly, however, hypothalamic levels of vasoconstrictor prostanoids (TXA 2 and PGF 2α ) decreased after chronic NOS blockade. COX inhibition by indomethacin but not by diclofenac decreased the HBF in control animals. However, neither indomethacin nor diclofenac induced an altered HBF-response after chronic L-NAME treatment. Although urinary excretion of PGI 2 and PGE 2 metabolites markedly increased during chronic NOS blockade, indicating COX activation in the systemic circulation, we conclude that the adaptation of the hypothalamic circulation to the reduction of NO synthesis is independent of vasodilator prostanoids. Reduced release of vasoconstrictor prostanoids, however, may contribute to the normalization of HBF after chronic loss of NO.

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Prostacyclin and prostagladin synthesis in isolated brain capillaries

Cited by 66 publications

References 18 publications

Arachidonic acid and prostaglandin endoperoxide metabolism in isolated rabbit and coronary microvessels and isolated and cultivated coronary microvessel endothelial cells.

Arachidonic acid and prostaglandin endoperoxide metabolism in isolated rabbit and coronary microvessels and isolated and cultivated coronary microvessel endothelial cells.

<I>Immunohistochemical Localization of Prostaglandin F<SUB>2α</SUB> in Reperfused Gerbil Brain</I>

Adaptation of the hypothalamic blood flow to chronic nitric oxide deficiency is independent of vasodilator prostanoids

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