Thromboxane B2 in borderline and essential hypertensive patients

Hornych, A; Safar, Michel E.; Bariéty, J; Simon, Alain; London, Gérard M.; Levenson, Jaime

doi:10.1016/s0262-1746(83)80005-5

Cited by 21 publications

(11 citation statements)

References 8 publications

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“…In the present study, we found no absolute differences between the urinary excretion of these eicosanoids in mild hypertensive and control subjects. The similar TXB 2 excretion rates in hypertensive and normotensive groups differs from findings reported by Hornych et al, 37 who found increased TXB 2 excretion in patients with mild essential hypertension and is in agreement with the findings of Campbell et al 34 who observed no consistent difference between urinary TXB 2 excretion in normal subjects and hypertensive patients. In view of the unimodal distribution of blood pressure in the population, 38 it is somewhat arbitrary to divide individuals into distinct hypertensive and normotensive groups.…”

Section: Mcgiff and Vanesupporting

confidence: 90%

Prostacyclin and thromboxane biosynthesis in mild essential hypertension.

et al. 1990

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The possibility that prostacyclin or thromboxane biosynthesis is abnormal in patients with established mild essential hypertension was investigated in 46 patients. These eicosanoids have opposing effects both on vascular smooth muscle and on platelets. An imbalance in their biosynthesis could therefore influence both vascular tone and predisposition to thrombosis. We studied the relation between blood pressure and the biosynthesis of prostacyclin and thromboxane A 2 by measuring urinary excretion rates of stable breakdown products of prostacyclin (6-oxo-prostaglandin F la and 2,3-dinor-6-oxo-prostaglandin F,J and of thromboxane A 2 (thromboxane B 2 and 2,3-dinor-thromboxane B 2 ) using immunoafnnity chromatography and gas chromatography/electron capture mass spectrometry. Excretion rates of both of the prostacyclin-derived products ranged from less than 5 to more than 100 ng/g creatinine; each was significantly negatively correlated with blood pressure (r=0.36-0.45). A reduction of 2,3-dinor-6-oxo-prostaglandin F, a excretion of 100 ng/g creatinine was associated with an increase in arterial pressure of 14 mm Hg (systolic) and 8 mm Hg (diastolic) in patients who had been without antihypertensive medication for 2 weeks. The same reduction in 6-oxo-prostaglandin F la excretion was associated with an increased pressure of 19 mm Hg (systolic) and 12 mm Hg (diastolic) (2p<0.05 for diastolic pressure and 2p<0.01 for systolic pressure in each case). There were similar correlations between the excretion rates of these products and blood pressure in the same patients while they were receiving antihypertensive therapy. In contrast, excretion rates of thromboxane B 2 and 2,3-dinor-thromboxane B 2 were not significantly correlated with blood pressure. We conclude that prostacyclin biosynthesis is selectively impaired in mild essential hypertension. This could contribute to the raised peripheral resistance and increased incidence of thrombosis that are characteristic of essential hypertension. {Hypertension 1990;15:469-474) E stablished essential hypertension is characterized by increased peripheral resistance 1 and an increased incidence of arterial occlusive disease.2 The pathophysiology of these processes is incompletely understood, but abnormal prostaglandin synthesis has been implicated. 3- 4 We have investigated the possible involvement of prostacyclin (PGI 2 ) or thromboxane A 2 (TXA 2 ). These eicosanoids are each formed from arachidonic acid but have opposing effects on platelets and vascular smooth muscle.5 PGI 2 is synthesized by vascular

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Section: Mcgiff and Vanesupporting

confidence: 90%

Prostacyclin and thromboxane biosynthesis in mild essential hypertension.

et al. 1990

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“…13 However, any abnormality in PGI 2 and TXA 2 biosynthesis in human hypertension has proved to be more difficult to assess. Whereas increased TXB 2 excretion in patients with essential hypertension has been reported, 14 other studies have found no such difference between hypertensive and normotensive individuals. 1516 We found that mean excretion of 2,3-dinor-6-oxo-PGF lo and 6-oxo-PGF la is similar in patients with mild essential hypertension and in normotensive subjects but that in hypertensive patients there is a negative correlation between blood pressure and these products of PGI 2 biosynthesis.…”

Section: Cgiffand Vanementioning

confidence: 80%

Thromboxane A2 receptor antagonism and synthase inhibition in essential hypertension.

et al. 1993

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Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart On each occasion, they received two doses of either placebo or ridogrel (300 rag) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A 2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B 2 , 6-oxoprostaglandin F lo , and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A 2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B 2 and thromboxane Bj compared with placebo (21 ±6 versus 279±28 and 14±4 versus 39±9 ng/g creatinine, respectively, P<.0001 and P<.05). Excretion of 2,3-dinor-6-oxoprostaglandin F 1(r and 6-oxoprostaglandin F, o was increased by ridogrel compared with placebo (184±20 versus 146±11 and 86±9 versus 58±6 ng/g creatinine, respectively; P<.0S). Ridogrel selectively antagonized platelet aggregation to the thromboxane mimetic (P<.0001). Blood pressure did not differ significantly between ridogrel and placebo treatment periods. Thus, in patients with essential hypertension, acute administration of ridogrel reduces renal and extrarenal thromboxane A 2 biosynthesis, increases renal and extrarenal prostacyclin biosynthesis, inhibits thromboxane receptor-activated platelet aggregation, but has no effect on systemic arterial pressure. (Hypertension 1993^22:197-203)

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“…Circulating 6KPGFla was found to be reduced in pa tients with essential hypertension in compar ison to normotcnsive patients [4], and TxB2 to be significantly higher in hypertensive pa tients than in controls [5]. Furthermore, it was suggested that a deficiency in local pros taglandin vasodilator release and possibly increased thromboxane synthesis, particu larly in the kidneys, contributed to the pro cess of essential hypertension [6].…”

Section: Discussionmentioning

confidence: 99%

“…However, it also ex tends the scope of the investigation, to exam ine the relationship of psychological to phys iological variables. Since there is evidence that abnormalities in prostaglandin PG12 (a vasorelaxant) and thromboxane (a vasocon strictor) may contribute to the palhophysiol-ogy of hypertension [4][5][6][7], an attempt was made to correlate them with hostile person ality characteristics. A recent investigation had examined similar correlations in a study of primary dysmenorrhea [8].…”

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confidence: 99%

Hostile Personality Characteristics and Prostaglandins in Essential Hypertension

Aritzi

Demakis

et al. 1989

Psychother Psychosom

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The hostile personality characteristic of dominance was shown to be significantly lower in a group of 34 male patients with essential hypertension than in a general illness control group (n = 17) in the USA. This replicates a previous finding from research in Greece into this and other conditions of presumably psychogenic origin. Nonspecific neurotic syndromes (as identified by the Present State Examination, a semistructured interview) were more prevalent in hypertensives than in controls, but no clear neurotic cases were found. Levels of the prostaglandins 6-keto prostaglandin F1A and thromboxane B₂ did not differ significantly between groups, but the former was positively correlated with dominance in the control group. An interpretation of these results in terms of the repressed hostility theory is offered.

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Thromboxane B2 in borderline and essential hypertensive patients

Cited by 21 publications

References 8 publications

Prostacyclin and thromboxane biosynthesis in mild essential hypertension.

Prostacyclin and thromboxane biosynthesis in mild essential hypertension.

Thromboxane A2 receptor antagonism and synthase inhibition in essential hypertension.

Hostile Personality Characteristics and Prostaglandins in Essential Hypertension

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