Thromboxane Generation in Patients with Essential Hypertension or Cerebrovascular Disease and Effect of Oral Aspirin

Matsumoto, Masahiro; Nukada, Tadaatsu; Uyama, Osamu; Yoneda, Shotaro; Imaizumi, Mitsuyoshi; Miyamoto, Terumasa; Kayama, N

doi:10.1055/s-0038-1650072

Cited by 15 publications

(6 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also found no consistent difference between urinary TxB 2 excretion between normal subjects and hypertensive patients. Our data thus agree with a recent report 14 of normal generation of TxB 2 by platelets from hypertensive patients.…”

Section: Discussionsupporting

confidence: 94%

“…The PGF 2(I excretion rates are of interest in hypertension, however, not only because of the possible suppressive effect of PGF^ upon renin release 9 but also because alterations in the ratio of PGEj/PGF^, reported with changes in dietary sodium, 12 may reflect alterations in the activity of PGE 2 -9-keto reductase, an enzyme that may metabolize PGE 2 . Thromboxane A 2 , a potent vasoconstrictor, 13 has been assessed only in an initial fashion 14 in patients with essential hypertension. Although animal studies 15 ' l6 have suggested a relationship between renal prostaglandin and kallikrein production, the changes in urinary kallikrein and prostaglandin excretion remain undefined in essential hypertension with changes in sodium status and during increased mineralocorticoid activity upon the kidney.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

et al. 1982

View full text Add to dashboard Cite

SUMMARY A deficiency in renal prostaglandins has been implicated in the pathogenesis of essential hypertension, particularly low renin hypertension. Previous studies of urinary prostaglandins as influenced by sodium balance and in essential hypertension have been handicapped by problems with assay methodology, inclusion of male subjects, and/or failure to standardize daily fluid consumption. We compared urinary excretion of prostaglandin E 2 (PGE,), prostaglandin F^ (PGF^), and thromboxane B 2 (TxB 2 ) in black and white normotensive and low-renin and normal-renin hypertensive women during two protocols producing sodium depletion (10 mEq sodium diet) and sodium loading (200 mEq sodium diet plus the fludrohydrocortisone Florinef, a synthetic mineralocorticoid). A constant fluid, potassium, and caloric intake was maintained throughout. Changes in plasma renin activity, urinary aldosterone excretion, and urinary kallikrein excretion were simultaneously assessed.As sodium intake decreased from 120 to 10 mEq sodium/day, increases in urinary PGF^ (502 ± 60 to 1222 ± 176 ng/24 hr, p < 0.01) and TxB ; (99 ± 33 to 216 ± 77 ng/24 hr, p < 0.05) excretion were observed in normotensive subjects. These increases were not observed in the hypertensive patients, possibly because less renin stimulation was achieved during the low sodium diet. Alternatively, subnormal prostaglandin production may have contributed to the lesser renin stimulation. Furthermore, urinary PGF, excretion in hypertensive patients during sodium depletion indicated strong influences of race and renin status; namely, black and normal-renin hypertensives increased urinary PGF^ excretion during sodium depletion whereas white and low-renin hypertensives did not. When white hypertensives and normotensive subjects consumed either 120 or 200 mEq sodium diet, there were no consistent differences in urinary excretion of PGE 2 , PGF^, or TxB 2 . With sodium loading, urinary PGE,, PGF^, and TxB 2 excretion did not change, whereas urinary kallikrein excretion increased. Urinary excretion of these prostanoids was therefore independent of mineralocorticoid and kallikrein effects upon the kidney. Thus, we found no evidence for a role of renal PGE 2 , PGF^, and TxB 2 in natriuresis in humans. Urinary excretion of these prostanoids was decreased in hypertensive patients only during sodium depletion. (Hypertension 4: 735-741, 1982) KEY WORDS • prostaglandins • thromboxane • kallikrein • renin • aldosterone natriuresis • mineralocorticoid escape • sodium loading

show abstract

Section: Discussionsupporting

confidence: 94%

mentioning

confidence: 99%

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

et al. 1982

View full text Add to dashboard Cite

show abstract

“…Several studies have previously reported increased platelet aggregability to AA in cerebrovascular disease. 26,27 Why sleep-awake fluctuation in platelet aggregability was confined to assays employing AA is uncer-tain. Platelet AA metabolism is subject to modulation by circulating catecholamines.…”

Section: Discussionmentioning

confidence: 99%

Platelet Aggregability in Sleep-Related Stroke

Voll

Chetty²,

Atkinson³

1989

Can. j. neurol. sci.

View full text Add to dashboard Cite

ABSTRACT:We examined platelet aggregability during nocturnal sleep and daytime wakefulness in patients with a history of sleep-related stroke onset (SOS) and compared it to that of matched awake-onset stroke (AOS) patients and controls without evidence of vascular disease. Aggregability was evaluated in-vitro at least seven weeks following stroke onset. Platelets were more aggregable to ADP, collagen and arachidonic acid (AA) during both sleep and wakefulness in patients with AOS (p<0.01). No significant difference in the mean aggregation thresholds during sleeping or waking periods were found between SOS and control groups. However, platelets were significantly more responsive to AA during sleep than during wakefulness in the SOS patients (p<0.01). This difference was confined to the subgroup of SOS patients who had experienced nocturnal as opposed to daytime sleep-related stroke onset, suggesting that the observed difference in platelet responsiveness to AA may be related to a circadian fluctuation in platelet aggregability rather than to a sleep-related fluctuation. Significant sleep-related changes in platelet aggregability were not identified in the other two groups.

show abstract

“…Notwithstanding this different sensitivity to the aggregating capacity of arachidonic acid, the amount of thromboxane B2 formed from 14C-arachidonic acid or 14C-PGH2 by washed platelets was similar in hypertensives (n = 40 and n = 40) and in controls (n = 26 and n --26) [24,52].…”

Section: Platelet Adhesion/aggregationmentioning

confidence: 91%

“…However, the amount of thomboxane B2 (TXB2) produced by washed platelets from either 14C-arachidonic acid or 14C-PGH2 did not differ significantly in hypertensive patients (n = 40) compared with normal controls (n = 26), suggesting that the platelet cyclooxygenase or thromboxane A2 synthetase activities are not modified in hypertension [24,52]. Similarly, the concentrations of TXB2 detectable in venous plasma were comparable in hypertensives (106.4 + 9.9 pg/ml; n = 12) and in norrnotensive controls (111.5 + 6 pg/ml; n = 22), indicating that excessive systemic activation of the platelet eicosanoid system, detectable in systemic blood, does not occur in this disease [55].…”

Section: Piatelet Arachidonic Acid Metabolitesmentioning

confidence: 99%

Blood platelets in human essential hypertension

1986

Agents and Actions

View full text Add to dashboard Cite

Blood platelets of patients with essential hypertension display signs of both increased sensitivity in vitro to aggregating stimuli believed to contribute to thrombosis and of activation in vivo possibly expressing the release of vasoactive products. The mean features of the modified platelet profile in hypertension include an increased alpha 2-adrenergic receptor density, an enhanced rate of adhesion/aggregation in particular in response to ADP and arachidonic acid, a greater sensitivity for thrombin and adrenaline to stimulate increases in cytoplasmic-free Ca2+, increased resting levels of cytoplasmatic-free Ca2+, a reduced content of serotonin often combined with a defective uptake mechanism, a facilitated efflux rate of noradrenaline, an exaggerated release reaction in vivo as indicated by the increased plasma levels of Beta-thromboglobulin and a shortened platelet life span. These changes occur to various extents in some, but not all, hypertensive patients and are not always strictly related to the degree of blood pressure increase. On the contrary, platelet cyclooxygenase and thromboxane synthetase activity are in the normal range.

show abstract

Thromboxane Generation in Patients with Essential Hypertension or Cerebrovascular Disease and Effect of Oral Aspirin

Cited by 15 publications

References 13 publications

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

Platelet Aggregability in Sleep-Related Stroke

Blood platelets in human essential hypertension

Contact Info

Product

Resources

About