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

Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-keto-PGF1 alpha (6-O-PGF1 alpha), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1 alpha. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1 alpha excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2 production is a pathogenetic factor in salt-induced hypertensive patients. In contrast, PGI2 may be produced adaptively to regulate blood pressure during changes in salt balance.
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PMID:Involvement of endogenous prostaglandins in salt-induced hypertension. 388 81

Sensitivity to adrenaline-antagonism of the inhibitory effect of PGI2 on thrombin-induced increase in [Ca2+]i was measured in platelets from normotensive and untreated hypertensive subjects. Platelets from hypertensive subjects exhibited an increased sensitivity to adrenaline. This effect was more pronounced in younger patients with hypertension, and suggests an increased adenylate cyclase sensitivity in the early hypertension. The data also indicate that a mechanism linked to calcium-influx plays an important role in older hypertensives. This may explain the greater efficacy of calcium entry blockers in older hypertensive patients with essential hypertension.
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PMID:Hormonal modulation of intracellular free calcium in platelets from normotensive and hypertensive subjects. 388 86

The interaction of inhibition of prostaglandin (PG) synthesis by indomethacin (75 mg/day) with the antihypertensive effect of atenolol (50 mg b.i.d.) was studied in 11 untreated otherwise healthy men 35 to 45 years old with essential hypertension. Atenolol for 3 weeks decreased supine blood pressure (BP) from 157/109 mm Hg during placebo to 148/97 mm Hg. Indomethacin alone for 1 week slightly increased BP and antagonized the antihypertensive action of atenolol. Atenolol reduced plasma renin activity (PRA) to 40% but did not modify either the urinary excretion of vasodilatory PGs (PGE2 and prostacyclin measured as 6-keto-PGF1 alpha) or plasma kininogen and urine kallikrein. Indomethacin suppressed PRA to 27% and PG excretion to approximately 70% but did not markedly change plasma kininogen and urine kallikrein excretion. The decreased excretion of 6-keto-PGF1 alpha, the metabolite of the main vasodilatory prostanoid prostacyclin, correlated with the increased BP measured in standing subjects. The effects of indomethacin were practically the same when given with atenolol as when given alone. We conclude that the slight increase in BP by indomethacin in essential hypertension is associated with the reduced production of vasodilatory PGs but not with alterations in activities of the renin-angiotensin or kallikrein-kinin systems.
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PMID:Inhibition of prostaglandin synthesis by indomethacin interacts with the antihypertensive effect of atenolol. 389 59

A large body of evidence supports the concept that prostaglandins (PG) are importantly involved in arterial pressure regulation. Various PGs, especially PGE2 and prostacyclin (PGI2) may influence blood pressure through control of vascular tone, sodium excretion, and renin release. Inhibition of PG synthesis by nonsteroidal antiinflammatory drugs (NSAID) augments the vasoconstrictor response to exogenous pressors such as angiotensin II, arginine vasopressin (AVP), and fludrocortisone. The acute administration of NSAID to either normotensive or untreated hypertensive subjects results in an increase in arterial pressure and peripheral resistance; long-term administration, however, is associated with little or no change in blood pressure, possibly because of a reduction in cardiac output. Although NSAID have little influence on blood pressure in normotensive subjects or untreated hypertensives, inhibition of PG synthesis blunts or abolishes the antihypertensive effect of most antihypertensive agents. NSAID antagonize the vasodepressor action of diuretics, beta-adrenoreceptor antagonists, vasodilators, and converting enzyme inhibitors. Consequently, potent NSAID should be used with caution, if at all, during treatment of hypertensive patients. Numerous studies have examined renal PG production in essential hypertension (EH). The majority have demonstrated reduced basal and stimulated urinary PGE2 excretion in EH compared to normotensive subjects, but there is substantial overlap. Nevertheless, renal PGE2 synthesis is significantly decreased in approximately one-third of patients with EH. A recent innovative approach to arterial pressure regulation has focused on dietary supplementation with polyunsaturated fatty acids (PUFA), especially linoleic acid and eicosapentaenoic acid. Several groups have demonstrated that long-term dietary supplementation with PUFA reduces blood pressure in both normotensive individuals and in patients with EH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of prostaglandins in human hypertension. 392 18

Prostaglandins (including PGE1, PGE2 and PGI2) showed little or no effect on Na+ and K+ transport across human red cell membranes. Conversely, they were able to: i) inhibit Na+, K+ cotransport system, ii) stimulate Na+, K+-pump and iii) stimulate Na+, Ca2+ exchange in mouse macrophages. These effects which seem to be mediated by cyclic AMP, provoke a more rapid extrusion of a cell Na+ -load. This may counterbalance the abnormal cell Na+ regulation that appears to be associated with essential hypertension.
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PMID:Ion transport, prostaglandins, and essential hypertension. 609 31

Prostacyclin production in neonates born at various gestational ages (28 weeks to term) was compared with that in neonates born of pregnancies complicated by various acute and chronic placental insufficiency states. Prostacyclin levels were reflected by the amount of conversion of 14C arachidonic acid to 6-keto-PGF1 alpha (the stable end-product of prostacyclin) by umbilical arteries. The uptake of 14C arachidonic acid by the umbilical arteries was also determined, and since this was similar for all groups it was not the cause of the differences noted in prostacyclin production. Neonates born of normal pregnancies had similar levels of prostacyclin production regardless of gestational age. Prostacyclin production was very low in neonates born of pregnancies complicated by chronic placental insufficiency (intrauterine growth retardation, essential hypertension, and pre-eclampsia), but normal with acute placental insufficiency (abruptio placentae). Hence the decrease in fetal prostacyclin production in pre-eclampsia is not related to gestational age; furthermore, it is also seen in other chronic placental insufficiency states.
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PMID:Decrease prostacyclin production: a characteristic of chronic placental insufficiency syndromes. 611 87

To determine whether prostaglandins contribute to the depressor response to the converting enzyme inhibitor, captopril, we measured the plasma prostaglandin levels by radioimmunoassy before and after captopril administration, and then examined the effect of prostaglandin synthetase inhibition on captopril's antihypertensive effect. When a single oral captopril dose (25-100 mg) was given to 31 sodium-restricted patients with essential hypertension, the levels of the stable transformation product of prostacyclin remained unmeasurable and that of thromboxane A2 did not change, while the metabolite of PGE2 (PGE-M) increased by 53% (34 +/- 4pg/ml pre-captopril, 52 +/- 5 pg/ml after; p less than 0.001). As expected, blood pressure (BP) and angiotension II (AII levels fell, and kinin levels rose (all changes p less than 0.001). We then blocked prostaglandin synthesis in 18 of these subjects for 24 hours with either indomethacin (n = 10) or aspirin (n = 8) before repeating the captopril dose, to assess the importance of these PGE-M increments. The PGE-M responses to captopril were effectively blocked in nine of 10 subjects receiving indomethacin and four of eight receiving aspirin. In these 13 patients, the depressor response to captopril was significantly blunted (-20 +/- 3mm Hg pre-synthetase inhibition vs - 13 +/- 2 mm Hg post; p less than 0.05). When these agents did not block the PGE-M response to captopril, the BP response was also unchanged (-15 +/- 4mm Hg pre, -18 +/- 5mm Hg post). Neither indomethacin nor aspirin changed the AII or kinin responses to captopril. We conclude that the prostaglandins may be important mediators of captopril's antihypertensive effect in the sodium-restricted state.
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PMID:Contribution of prostaglandins to the antihypertensive action of captopril in essential hypertension. 626 Jun 45

The contribution, if any, of various prostaglandins to the antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) is controversial. We studied the effect of the ACEI captopril (CAP) on the urinary excretion of 6-keto-PGF2 alpha (6-KF), the major metabolite of the vasodilatory prostaglandin, prostacyclin, and thromboxane B2 (TxB2), the stable metabolite of the vasoconstrictor TxA2, in 8 patients with essential hypertension after placebo, two weeks of CAP 25 mg t.i.d. alone, and the same dose of CAP in combination with hydrochlorothiazide (HCTZ) 50 mg/day. Mean 6-KF and TxB2 (nmol/8 hr post-dosing, respectively) did not differ significantly with any treatment; the mean ratio of 6-KF/TxB2 was also unchanged. Likewise, the excretion of these prostaglandins was also evaluated after placebo, the ACEI enalapril (ENA) (5 or 10 mg/day), and the combination of ENA and HCTZ in another group of 8 patients with essential hypertension. Mean 6-KF and TxB2 (nmol/24 hr post-dosing, respectively) showed no significant treatment-related differences; the mean ratio was again unchanged. No correlation existed between the magnitude of blood pressure responses with any treatment and either 6-KF or TxB2 excretion. Thus, the antihypertensive action of ACEI, alone or in combination with HCTZ, does not appear to involve alterations in these vasoactive prostaglandins.
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PMID:Urinary excretion of prostacyclin and thromboxane A2 metabolites after angiotensin converting enzyme inhibition in hypertensive patients. 630 85

To assess the pathophysiological role of prostacyclin in essential hypertension, plasma levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable, nonenzymatic metabolite of prostacyclin, were assayed in 25 patients with essential hypertension and 25 age-matched normotensive subjects. Supine plasma levels of 6-keto-PGF1 alpha were 270 +/- 14 (SE) in normotensive subjects and 203 +/- 14 pg/ml in the patients with essential hypertension. The difference was statistically significant (p less than 0.001). There was a significant negative correlation between plasma levels of 6-keto-PGF1 alpha and systolic blood pressure (r = 0.44, P less than 0.002), diastolic blood pressure (r = 0.55, p less than 0.001), or mean blood pressure (r = 0.56, p less than 0.001) in the pooled subjects. The same relationship was found in the hypertensive patients. There was no definite relationship either between plasma levels of 6-keto-PGF1 alpha and plasma renin activity (PRA) in the supine position, or between changes in plasma levels of 6-keto-PGF1 alpha and changes in PRA after 60 min of upright posture. These results indicate that circulating prostacyclin is reduced in patients with essential hypertension as compared to normotensive subjects. This reduction of plasma prostacyclin may participate, in part, in the maintenance of blood pressure elevation in patients with essential hypertension. It is also suggested that upright posture is not sufficient to elevate circulating prostacyclin.
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PMID:Plasma levels of 6-keto-prostaglandin F1 alpha in normotensive subjects and patients with essential hypertension. 634 3

To assess the pathophysiological role of prostacyclin in essential hypertension, plasma levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF 1 alpha), a stable, nonenzymatic metabolite of prostacyclin, were assayed in 25 patients with essential hypertension and 25 age-matched normotensive subjects. Supine plasma levels of 6-keto-PGF1 alpha were 270 +/- 14 (SE) in normotensive subjects and 203 +/- 14 pg/ml in the patients with essential hypertension. The difference was statistically significant (p less than 0.001). There was a significant negative correlation between plasma levels of 6-keto-PGF1 alpha and systolic blood pressure (r = -0.44, P less than 0.002), diastolic blood pressure (r = -0.55, p less than 0.001), or mean blood pressure (r = -0.56, p less than 0.001) in the pooled subjects. The same relationship was found in the hypertensive patients. There was no definite relationship either between plasma levels of 6-keto-PGF1 alpha and plasma renin activity (PRA) in the supine position, or between changes in plasma levels of 6-keto-PGF1 alpha and changes in PRA after 60 min of upright posture. These results indicate that circulating prostacyclin is reduced in patients with essential hypertension as compared to normotensive subjects. This reduction of plasma prostacyclin may participate, in part, in the maintenance of blood pressure elevation in patients with essential hypertension. It is also suggested that upright posture is not sufficient to elevate circulating prostacyclin.
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PMID:Plasma levels of 6-keto-prostaglandin F1 alpha in normotensive subjects and patients with essential hypertension. 634 3


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