Interactions Between Nitric Oxide and Prostacyclin

Gryglewski, Ryszard J.

doi:10.1055/s-2007-994020

Cited by 37 publications

(17 citation statements)

References 78 publications

(99 reference statements)

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“…When RPP was increased stepwise from 90 to 150 mmHg, inhibition of the NO synthase by L-NAME did not modify the filtration fraction since the induced changes in by use of micropuncture techniques in the rat (Zatz & De Nucci, 1991) and rabbit (Denton & Anderson, 1994 Wang & Voelkel (1989) that prostanoid synthesis was not tightly coupled with the magnitude of the contraction. Therefore, the most likely explanation is that NO directly modifies the phospholipase A2 or more, probably, the cyclooxygenase activity (Gryglewski, 1993) and inhibits the release of TxA2 and PGH2. This hypothesis is supported by the finding that L-NAME markedly activated the synthesis of TxB2 at any RPP level studied.…”

Section: Resultsmentioning

confidence: 99%

Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat

Ziyyat

Zhang

Benzoni

1996

British J Pharmacology

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1 The present study was aimed to assess the interaction between nitric oxide (NO) and thromboxane (Tx) A2-prostaglandin (PG) H2 in single-pass perfused isolated kidneys of the rat.2 Noradrenaline (NA, 63 and 110 nM) dose-dependently elevated the renal vascular resistance (RVR), the glomerular filtration rate (GFR) and the urinary excretion of sodium (UNaV). Infusion of Nw-nitro-Larginine methyl ester (L-NAME, 100 gM), an inhibitor of NO synthesis, enhanced the effects of NA on RVR and on UNaV, but decreased those on GFR. The TxA2-PGH2 (TP) receptor blockade by GR32191B (10 gM) attenuated this potentiating effect of L-NAME.3 When renal perfusion pressure was stepwise increased from 90 to 150 mmHg, L-NAME similarly decreased renal perfusion flow rate and GFR. 4 The venous excretion of TxB2 and 6-keto-PGF,c, was increased by L-NAME in baseline conditions as well as after NA or increasing renal perfusion pressure (RPP). 5 These results suggest that: (1) TxA2 and PGH2 play an important role in the overall effect of the renal prostanoids, (2) NO strongly interacts with the cyclo-oxygenase pathway and reduces the prostanoid synthesis in the kidney, and (3) the pressor effect of L-NAME partly relies upon the vasoconstrictor effect of TxA2 and PGH2.

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Section: Resultsmentioning

confidence: 99%

Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat

Ziyyat

Zhang

Benzoni

1996

British J Pharmacology

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“…It is recognized that the intact endothelium produces a variety of substances, including NO, tPA and prostacyclin, that are physiologically important to the local blood flow, as well as ensuring both the maintenance of a nonthrombogenic surface and facilitating local clot lysis. 92,95,96 As noted, "antiplatelet" agents such as aspirin may affect both NO and prostacyclin levels, with resultant adverse effects on exogenous tPA therapy. It is also recognized that the clinical use of tPA as a monotherapy for acute stroke will remain limited.…”

Section: Future Directionsmentioning

confidence: 99%

Antiplatelet Therapy in Acute Cerebral Ischemia

Bednar

Gross

1999

Stroke

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Background-Improved recognition of stroke signs and symptoms has paralleled the development of pharmacological strategies that may be examined to reduce stroke mortality and morbidity. Presently, tissue plasminogen activator is the only therapy that significantly improves outcome in acute stroke, with no agent demonstrating a significant reduction in mortality. Summary of Review-Antiplatelet agents are a heterogenous class of drugs that have been successfully used for more than 2 decades in secondary stroke prevention. These agents include aspirin, with or without dipyridamole, and more recently, the adenosine antagonists ticlopidine and clopidogrel. However, studies of the use of antiplatelet agents within 48 hours of the ictus have examined only aspirin. Only 1 study, the Multicentre Acute Stroke Trial-Italy (MAST-I), entered patients within 6 hours of the ictus. These data suggest that an improvement in mortality may be related to the speed of administration. No significant adverse events were noted with early antiplatelet monotherapy. However, MAST-I did note a significant increase in early mortality in patients receiving aspirin plus streptokinase, a finding not adequately explained by an increase in the intracranial hemorrhage rate. Conclusions-The use of antiplatelet therapy in acute stroke, clinical or experimental, has only recently received attention.It is likely that the use of antiplatelet agents for acute stroke therapy will be less restrictive than that currently seen for thrombolytics. Future studies should include an examination of those agents that have previously demonstrated efficacy in secondary stroke prevention, most notably, aspirin. The recognition that all platelet stimuli share a final common pathway that is dependent on the surface glycoprotein IIb/IIIa (fibrinogen) receptor has resulted in the development of various agents which block this receptor and are currently the focus for clinical trials. The role of nitric oxide in stroke therapy will depend on minimizing the hypotensive side effects of this agent. Stroke models are needed to provide preliminary data on the efficacy of antiplatelet therapy, especially as relates to the interaction of antiplatelet agents with thrombolytics. (Stroke. 1999;30:887-893.)

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“…Although chemically different, prostacyclin and NO are interlinked in many ways. Their biologic activities are similar [8]and they interfere with the release of each other [8, 9, 10]. Both prostacyclin and NO counteract platelet aggregation [10, 11, 12]and inhibit platelet and leukocyte adhesion to the vessel wall [13, 14, 15].…”

Section: Introductionmentioning

confidence: 99%

Role of Prostacyclin and Nitric Oxide in Regulation of Basal Microvascular Hydraulic Permeability in Cat Skeletal Muscle

Möller

Grände²

1999

J Vasc Res

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The effects of prostacyclin, nitric oxide (NO) and β₂-receptor stimulation on capillary filtration coefficient (CFC) and vascular tone were analyzed in an autoperfused cat skeletal muscle in vivo preparation, to evaluate if these substances are involved in regulation of basal microvascular hydraulic permeability. CFC was increased from control (100%) to 124% with the prostacyclin-synthase inhibitor tranylcypromine and restored by simultaneous infusion of prostacyclin at 0.1 ng·kg^–1· min^–1, with further reduction to 76% at 1 ng· kg^–1·min^–1. Prostacyclin at these doses did not influence vascular tone. NO inhibition by L-NAME increased CFC to 116% of control, with a vascular resistance increase of 45%. CFC was restored by simultaneous infusion of the NO precursor L-arginine. L-arginine given alone reduced CFC to 86% of control. Tranylcypromine and L-NAME given together increased CFC to 141% of control and CFC was reduced to 86% by prostacyclin at 1 ng·kg^–1·min^–1 with no significant further reduction by adding L-arginine. Adrenaline alone, in a vasodilating dose verifying β₂ stimulation, or when followed by simultaneous β-blockade with propranolol, did not influence CFC. We conclude that NO and especially prostacyclin are involved in bi-directional regulation of basal microvascular hydraulic permeability and can account for up to 30–40% increase or decrease from a basal value. Physiological β₂ stimulation has no effect on basal hydraulic permeability. The permeability-reducing effects of prostacyclin and NO are additive. NO, but not prostacyclin, is involved in regulation of basal vascular tone.

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Interactions Between Nitric Oxide and Prostacyclin

Cited by 37 publications

References 78 publications

Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat

Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat

Antiplatelet Therapy in Acute Cerebral Ischemia

Role of Prostacyclin and Nitric Oxide in Regulation of Basal Microvascular Hydraulic Permeability in Cat Skeletal Muscle

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