Thromboxane A2 and development of genetic hypertension in the Lyon rat strain.

Geoffroy, J; Benzoni, Daniel; Vincent, Madeleine; Sassard, J

doi:10.1161/01.hyp.16.6.655

Cited by 17 publications

(8 citation statements)

References 27 publications

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“…It wasalso reported that the chronic administration of cyclosporine-A increased the TxA2 to PGI2 ratio (28), and that it diminished the production ofPGI2 in several vascular models (28). The effects ofTxA2on blood pressure have also been reported in animal experiments, where increased production of TxA2takes part in the systemic blood pressure regulation in spontaneously hypertensive rats (9) and Lyonstrain rats (10), which also suggests that the ratio of PGI2 to TxA2 can be considered as an index of vasodilating activities from the viewpoint of prostanoid metabolism.…”

Section: Discussionmentioning

confidence: 60%

“…Any stimulation of the arachidonate cascade such as via platelet activation potentially induces the increased vascular tone by TxA2in association with a decrease in the production of PGI2, resulting in pathologic stimulation coinciding with hypertension (9,10). Furthermore, OSASis accompanied by pulmonary hypertension and systemic hypertension in 1 0-20% (7, 1 1, 12) and 50-60% of all the cases (6)(7)(8)13), respectively.…”

Section: Introductionmentioning

confidence: 99%

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Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

et al. 1998

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Since obstructive sleep apnea syndrome (OSAS) is often linked with systemic hypertension, we sought to clarify the characteristics ofprostanoid metabolism in OSAS. In 7 OSASpatients (apneahypopnea index, 51.0 ± 23.4) and 7 non-snorers as control, nocturnal urine was sampled and analyzed for stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), [6-keto-PGFlot and thromboxane B2 (TxB2)]. The ratio of 6-keto-PGFl0C to TxB2 was significantly higher in OSAS (2.97 ± 1.52) than in control (1.38 ± 0.38). Successful treatment with nasal continuous positive airway pressure (8.3 ± 1.5 cmH2O)for 3 days caused a significant decrease in mean blood pressure in OSAS. Moreover, the 6-keto-PGFl0C to TxB2 ratio also significantly decreased to 1.74 ± 0.58, a level which may not significantly different from control. These results suggest that the production ratio of PGI2 to TxA2is shifted toward vasodilatation in untreated OSAS. Weconclude that the production of prostanoids plays a role in compensating for the systemic hypertension in OSAS.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

et al. 1998

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“…LH rats were treated orally from 3-9 weeks of age and their systolic BP measured by the tail-cuff technique. It ap peared [4] that both synthase inhibitors progressively and partially (-15 mm Hg) opposed the development of hy pertension in LH rats, the effects of OKY046 being more marked than those of Dazmegrel. The TP receptor block ade effects were as progressive but of greater magnitude than those of the TX synthase inhibitors.…”

Section: Renal Synthesis Of Eicosanoids In Genetically Hypertensive Rmentioning

confidence: 99%

Renal Eicosanoids and Blood Pressure in Genetically Hypertensive Rats of the Lyon Strain

Sassard¹,

Benzoni²

1994

J Biomed Sci

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The present paper reviews the evidence for a possible involvement of renal eicosanoids in the pathophysiology of high blood pressure in genetically hypertensive rats of the Lyon strain. Both in vivo and in vitro experiments suggest that an increased ability to synthesize the vasoconstrictor prostaglandin H(2) and/or thromboxane A(2) in renal vessels (1) acts as an autocrine amplifier of pressor agents and (2) may contribute to resetting the pressure natriuresis curve which is a prerequisite for the development and maintenance of hypertension.

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“…In genetically hypertensive rats of the Lyon strain (LH), an increase in renal TxAz synthesis has also been demonstrated in vivo (Geoffroy et al 1986) and in vitro using isolated perfused kidney (Liu et al 1991). Chronic Tx synthase inhibition and, more markedly, TxAz/ PGHz receptor blockade decreased blood pressure (BP) in LH rats (Geoffroy et al 1990). In SHR, the BP effects of chronic synthase inhibition or TxAz/ PGHz receptor antagonism have been mixed.…”

Section: Introductionmentioning

confidence: 99%

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

Boussairi¹,

Sacquet²,

Benzoni³

et al. 1993

Clin Exp Pharma Physio

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1. The effects of CGS 22652, a thromboxane (Tx) A2 synthase inhibitor and TxA2/prostaglandin (PG) H2 receptor antagonist, on blood pressure (BP) were studied in conscious freely moving spontaneously hypertensive rats (SHR). 2. Three groups of 13 male SHR were subcutaneously infused from 5 to 11 weeks of age via osmotic minipumps with CGS 22652 at doses of 5 (SHRa) or 10 (SHRb) mg/kg per 24 h or with the vehicle only (SHRc). A fourth group (SHRd, n = 13) was orally treated from 3 to 11 weeks of age with CGS 22652 (30 mg/kg) given by gavage once a day. 3. CGS 22652 dose-dependently reduced the age-related increase in systolic BP. The pressor response to noradrenaline (200 ng/kg, i.v.) but not to angiotensin I or II was slightly (P < 0.05) diminished in 11 week old SHRb and SHRd compared to SHRc. Acute ganglionic blockade by trimethaphan (10 mg/kg, i.v.), as well as angiotensin converting enzyme inhibition by perindopril (2 mg/kg, i.v.) decreased BP to a similar extent in the four groups. After combined blockade of vasopressin receptors and of the autonomic nervous system and the administration of a direct vasodilator (hydralazine, 3 mg/kg, i.v.), the residual mean BP was identical in the four groups of rats. 4. Chronic treatment with CGS 22652 dose-dependent antagonized the TxA2/PGH2 receptors but did not modify the TxA2 synthesis. The urinary sodium excretion did not differ between groups. 5. In conclusion, at the doses used, CGS 22652 given either orally or subcutaneously exhibited only TxA2/PGH2 receptor blocking properties in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

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Thromboxane A2 and development of genetic hypertension in the Lyon rat strain.

Cited by 17 publications

References 27 publications

Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

Renal Eicosanoids and Blood Pressure in Genetically Hypertensive Rats of the Lyon Strain

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

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Thromboxane A2 and development of genetic hypertension in the Lyon rat strain.

Cited by 17 publications

References 27 publications

Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

Compensatory Excretion of Prostacyclin and Thromboxane Metabolites in Obstructive Sleep Apnea Syndrome.

Renal Eicosanoids and Blood Pressure in Genetically Hypertensive Rats of the Lyon Strain

BLOOD PRESSURE EFFECTS OF THROMBOXANE A2 BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

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BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS