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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental radioisotopic study in normotensive male Wistar rats and spontaneously-hypertensive rats (SHR) of Okamoto--Aoki line demonstrated an age-related increase in the biosynthesis of prostacycline (PGI2) from 14C-arachidonic acid by pulmonary and aortal tissues of animals with normal arterial pressure. In SHRs, PGI2 production by lung homogenates did not change essentially with age, but decreased considerably in adult SHRs with stable hypertension. PGI2 biosynthesis by SHR's aortal tissue decreased with age and dropped significantly as arterial hypertension developed. In normotensive rats, the formation of thromboxane B2 (TxB2) by platelets increased with age. Platelet TxB2 biosynthesis was elevated considerably both in young and adult SHRs. Clinically, a significant increase of platelet TxB2 production from exogenous 14C-arachidonic acid was demonstrated in children with essential hypertension.
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PMID:[Age-related changes in prostacyclin and thromboxane B2 biosynthesis under normal conditions and in arterial hypertension]. 636 25

Much evidence has implied a deficient production of the antiaggregatory and vasodilator agent prostacyclin (PGI2) in preeclampsia and some other chronic fetoplacental insufficiency syndromes. So that we could study whether this might be due to the possible effects of the mode of delivery and maternal epidural or general anesthesia, specimens of the umbilical arteries of infants born after normal (n = 46) or complicated (n = 25) pregnancies were superfused in vitro and their production of PGI2 was determined by measuring 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, the hydrolysis product of PGI2) by radioimmunoassay. The amounts of umbilical 6-keto-PGF1 alpha released in normal pregnancies after induced vaginal delivery (20.9 +/- 2.4 ng/gm/min dry weight of tissue, mean +/- SEM) and elective cesarean section (21.8 +/- 2.2 ng/gm/min) were smaller (p less than 0.025) than the amounts released after spontaneous onset of labor (35.0 +/- 6.2 ng/gm/min). Epidural or general anesthesia had no effect on this production. When the types of deliveries were matched, the production of 6-keto-PGF1 alpha was even less (p less than 0.05) in cases of preeclampsia (14.2 +/- 3.7 ng/gm/min; n = 9) than in the control subjects (21.3 +/- 1.6 ng/gm/min) and in cases of essential hypertension (21.6 +/- 5.2 ng/gm/min). Our data suggest that umbilical PGI2 deficiency is a specific feature of preeclampsia.
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PMID:Evidence that prostacyclin deficiency is a specific feature in preeclampsia. 636 77

That adrenaline is involved in the pathophysiology of essential hypertension (EHT) is suggested by the observed elevation of plasma adrenaline concentration in some patients. Adrenaline, by stimulating the alpha-2 adrenoceptor, causes vasoconstriction in the smooth muscle cell and initiates shape change and aggregation in platelets. Therefore, the effect of adrenaline on intracellular free calcium concentration ([Ca2+]i) in the platelets of hypertensive subjects was investigated as a model for vascular smooth muscle. Platelets from untreated patients with EHT had an elevated [Ca2+]i and incubation with adrenaline for 30 min caused a greater increase in [Ca2+]i in treated patients with EHT than in normotensive controls. This long-term effect of adrenaline was possibly linked to a defective calcium extrusion mechanism in hypertension. No immediate effect was observed on [Ca2+]i by PGI2 and adrenaline, while both modulated [Ca2+]i if the platelets were stimulated with thrombin. PGI2 prevented the thrombin-induced increase in [Ca2+]i and adrenaline antagonized the effect of PGI2. Platelets from untreated patients with EHT exhibited an increased sensitivity to thrombin and adrenaline when compared to normotensive and treated hypertensive subjects. It is suggested that these supersensitivities are related to the elevated [Ca2+]i in untreated hypertensive patients.
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PMID:Free calcium response to adrenaline in platelets of normal and hypertensive (untreated and treated) subjects. 640 Mar 64

Plasma concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2), the stable nonenzymatic metabolites of prostacyclin and TXA2, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A2 (TXA2) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated. There were significantly increased plasma TXB2 concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF1 alpha concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF1 alpha and TXB2 and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values. These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA2 may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.
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PMID:Plasma concentrations of 6-keto-prostaglandin F1 alpha, thromboxane B2 and platelet aggregation in patients with essential hypertension. 654 1

Prostacyclin may act physiologically as an antihypertensive hormone. It remains uncertain, however, whether prostacyclin may be involved in the etiology of primary hypertension. As an index of prostacyclin production, we measured the levels of venous plasma 6-keto-PGF1 alpha by specific radioimmunoassay after silicic acid column chromatographic purification in 31 normotensive and 36 hypertensive males. The subjects were grouped according to the presence or absence of a family history of hypertension, and matched for age and blood pressure. Levels of 6-keto-PGF1 alpha in normotensive males with a family history of hypertension (12.0 +/- 1.7 pg/ml; mean +/- SEM; n = 18) were lower than in normotensive males without a family history of hypertension (17.7 +/- 2.0 pg/ml; n = 13) (p less than 0.01). Levels of plasma 6-keto-PGF1 alpha in hypertensive males with a family history of hypertension (10.2 +/- 1.2 pg/ml; n = 15) were lower than in hypertensive males without a family history of hypertension (20.5 +/- 1.5 pg/ml; n = 21) (p less than 0.005). The levels of plasma 6-keto-PGF1 alpha in males with a family history of hypertension may be decreased genetically. The decrease in production of prostacyclin in males with a family history of hypertension may be a factor in the etiology of hypertension.
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PMID:Levels of plasma 6-keto-PGF1 alpha in normotensive and essential hypertensive males with and without a family history of hypertension. 657 4

Recent publications have described increased vascular prostacyclin synthesis in vascular tissue from both spontaneous and experimental hypertensive animals and hypertensive humans. The only paper dealing with the platelet sensitivity reported that the cells are not abnormally sensitive to PGI2 in spontaneously hypertensive rats. In 22 patients with essential hypertension the platelet sensitivity to the antiaggregatory prostaglandins PGI2, PGE1, and PGD2 was studied on admission and two weeks after successful treatment with a beta-blocking agent. In all the age groups and in both sexes no differences in platelet sensitivity could be detected. These findings suggest that increased vascular PGI-2 synthesis is not counterbalanced by a change in platelet sensitivity in men.
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PMID:Hypertension and beneficial treatment with beta-blocking agents does not change the platelet sensitivity to the antiaggregatory prostaglandins. 675 58

To evaluate the role of the vasoactive prostaglandins prostacyclin and thromboxane A2 in essential hypertension, the stable metabolites 6-keto-PGF1 alpha and thromboxane B2, respectively, were measured in plasma before and after therapy in 7 patients. During the placebo phase, plasma 6-keto-PGF1 alpha levels were significantly greater than normal. Plasma thromboxane B2 levels were not statistically different from those in normal subjects. After intravenous administration of labetalol to the point of blood pressure reduction, neither plasma 6-keto-PGF1 alpha nor thromboxane B2 values changed. With prolonged oral labetalol therapy and concurrent regulation of blood pressure, a significant decrease in plasma 6-keto-PGF1 alpha levels occurred while thromboxane B2 values remained unaltered. Elevation of plasma 6-keto-PGF1 alpha in untreated hypertensive subjects suggests that enhanced vessel wall prostacyclin synthesis may be a protective mechanism to prevent organ damage. As blood pressure is controlled this increase is no longer needed, and prostacyclin generation returns to normal.
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PMID:Increased plasma concentrations of prostacyclin metabolite 6-keto-PGF1 alpha in essential hypertension. Influence of therapy with labetalol. 682 61

Essential hypertension, while considered to be idiopathic, may be due to a variety of physiologic and/or psychologic factors, including stress. A possible mechanism for stress-induced hypertension is the inhibition of prostaglandin (PG) synthesis by the release of corticoids in the stereotypical stress response. PGI2 and PGE2, acting as vasodilators are important antagonists to the pressor effects of norepinephrine. However, a decreased synthesis of these PGs due to higher cortisol levels associated with stress, would negate their vasodilatory action, thus favoring vasoconstriction due to vascular suprasensitivity to norepinephrine. PGF2 alpha, a vasoconstrictor thought to be synthesized in the brain in response to a stressor, may also play a key role in the pathogenesis of hypertension.
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PMID:Inhibition of prostaglandin synthesis: a possible mechanism for stress-induced hypertension. 687 21

A within-patient randomized, double-blind, crossover study was performed to investigate mechanisms of action of bendroflumethiazide in mild essential hypertension. Significant reductions in lying, standing, and postexercise blood pressure were seen after both 3 days and 10 wk treatment with bendroflumethiazide 10 mg daily. Plasma levels of 6-oxo-PGF1 alpha, the chemical hydrolysis product of prostacyclin, were increased by both 3 days and 10 wk therapy with bendroflumethiazide. This raises the possibility that thiazides may reduce peripheral resistance by increasing prostacyclin biosynthesis.
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PMID:Antihypertensive action of bendroflumethiazide: increased prostacyclin production? 700 30

1. Urinary excretion rate of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable nonenzymatic transformation product of prostacyclin (PGI2), was measured in 13 patients with sustained essential hypertension and in nine normotensive control subjects by a specific radioimmunoassay. 2. Patients with essential hypertension had significantly lower 6-keto-PGF1 alpha excretion rates irrespective of their sex, but in both groups urinary 6-keto-PGF1 alpha was lower in females. 3. Sodium excretion was significantly correlated with urinary 6-keto-PGF1 alpha only in hypertensive subjects. There was also a positive correlation between 6-keto-PGF1 alpha and urine volume in control subjects and in hypertensive patients. 4. If diminished urinary 6-keto-PGF1 alpha reflects suppressed endogenous PGI2 production, a deficiency in this important vasodepressor substance in essential hypertension may contribute to the pathogenesis of this disease.
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PMID:Diminished urinary prostacyclin metabolite in essential hypertension. 700 19


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