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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Renal prostaglandins act primarily as local hormones, having their effects at, or near to, sites of synthesis. PGE2 is a major determinant of renal vascular reactivity; it opposes the vasoconstrictor and natriuretic actions of pressor hormones and brakes the release of noradrenaline from adrenergic nerves. In the unanaesthetized rabbit prolonged inhibition of prostaglandin synthesis results in hypertension. In the rat, however, renal prostaglandins augment pressor stimuli. 2. Basal efflux of renal prostaglandins is positively correlated with blood flow to the inner cortex and medulla. Those stimuli which increase renal medullary blood flow do so primarily by activating prostaglandin synthetase. 3. Kinins increase prostaglandin synthesis which action modifies the renal effects of kinins. Thus, one or more renal prostaglandins contribute to the renal vasodilator action of bradykinin and mediate its effect on excretion of water as well as possibly attenuating the natriuretic action of the polypeptide. Kinins in addition to stimulating prostaglandin synthesis may determine the principal product of synthetase by regulating the enzyme PGE 9-ketoreductase, which converts PGE to PGF. The coupling of these systems within the kidney appears unique--prostaglandins mediate some of the actions of kinins and modulate others, whereas they depend on the intrarenal generation of kinins to set their level and type of activity.
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PMID:Renal prostaglandins. 82 36

Intrauterine (PGF) prostaglandin F2alpha (5 mg) was administered for termination of early pregnancy in 14 healthy volunteers. With 11 complete abortions, the efficiency rate of this technique is below conventional methods. In addition, the incidence of infection was high, occurring in 12 out of 14 subjects. Because of persistent bleeding, 6 patients underwent a dilatation and curettage. Other significant side effects included transient hypertension, pain, nausea, and restlessness. In the patients with a complete abortion, the mean plasma progesterone concentration fell 37% after 8 hours post-PGF2alpha instillation and 90% 14 days later. The mean plasma estradiol-17beta fell 26% over the initial 8 hour period and 75% over the next 14 days.
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PMID:Intrauterine instillation of prostaglandin F2ALPHA IN EARLY PREGNANCY. 116 90

In 127 healthy pregnant women of the 27th and 28th gestational week, the influence of somatic and affective disorders was investigated with regard to pregnancy-induced hypertension (PIH) after the 30th gestational week prospectively. The women answered a five step self-rating scale including 28 somatic and affective symptoms. The incidence of PIH achieved 12.7%. The PIH-group rated disorders significantly higher than the group without PIH (p less than 0.001). The self rated anxious hostile behaviour disorders were significantly stronger in the PIH-group than in the controls. So, in our sample anxious hostile behaviour appeared to be precursor of PIH. Somatic and affective symptoms of anxiety and hostility are provocated by adrenaline and noradrenaline typically. Catecholamines stimulate synthesis of prostaglandins, favouring PGF and TX. The resulting imbalance of prostaglandins appears to cause PIH pathognomonically. There is discussed that persisting anxious hostile behaviour is able to induce PIH by catecholamine-prostaglandin-mechanism.
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PMID:[Anxious hostile behavior as a precursor of pregnancy-induced hypertension]. 192 73

Little is known about the distribution of prostaglandin E2 (PGE2) and prostacyclin (PGI2) production in the canine kidney. To determine the basal and stimulated profiles of PGE2 and PGI2 production along the corticomedullary axis of the dog kidney, a slice (0.5 mm thick, 10-50 mg) was obtained from six equally spaced zones along the axis (zone 1, medullary crest; zones 2 and 3, inner medulla; zone 4, outer medulla; and zones 5 and 6, cortex) and was divided into equal halves. One half of the slice was incubated with Krebs-Ringer buffer containing arachidonic acid (6.6 x 10(-4) M), bradykinin (9.4 x 10(-6) M), or indomethacin (10(-5) M), whereas the remaining half of each slice was similarly incubated in Krebs-Ringer buffer alone. The production of PGE2 and 6-keto-PGF1 alpha (the stable metabolite of PGI2) was determined by radioimmunoassay. Under basal conditions, both PGE2 and 6-keto-PGF1 alpha were highest in the innermost zones of the inner medulla (PGE2, 3,328 +/- 549 pg/mg; 6-keto-PGF 1 alpha, 1,611 +/- 129 pg/mg) and decreased exponentially to low levels in the cortex (PGE2, undetectable; 6-keto-PGF1 alpha, 13 +/- 2 pg/mg); this production was inhibited by indomethacin. Arachidonic acid significantly increased the production of PGE2 in all zones of the kidney and the production of 6-keto-PGF1 alpha only in zones 3-6.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Distribution of prostaglandins E2 and 6-keto-F1 alpha production in dog kidneys. 210 67

We examined the contribution of endogenous prostanoids to baroreceptor activation in chronic renal hypertension. Baroreceptor activity was recorded from the vascularly isolated carotid sinus during slow ramp increases in pressure in rabbits anesthetized with pentothal and chloralose. Mean arterial pressure averaged 133 +/- 4 mmHg in hypertensive rabbits (one kidney, one wrap, n = 12) and 85 +/- 3 mmHg in normotensive rabbits (one kidney, no wrap, n = 13). Baroreceptor activity was decreased significantly (P less than 0.05) in the hypertensive compared with the normotensive rabbits. The decreased baroreceptor activity could not be explained by decreased distensibility of the carotid sinus (sonomicrometers). Inhibition of the endogenous formation of prostanoids with intrasinus administration of indomethacin (50 microM) decreased baroreceptor activity in normotensive (P less than 0.05) but not in hypertensive rabbits over a wide range of pressures. At a pressure of 120 mmHg, activity declined from 61 +/- 14 spikes/s before indomethacin to 47 +/- 12 spikes/s with indomethacin, i.e., a drop of 24 +/- 4%. In contrast, corresponding values in hypertensive rabbits averaged 41 +/- 13 and 40 +/- 12 spikes/s (-1 +/- 2%). Intrasinus prostacyclin, on the other hand, increased activity in both groups: at 120 mmHg activity increased from 62 +/- 9 to 92 +/- 15 spikes/s (51 +/- 17%) in normotensive rabbits and from 29+/- 7 to 47 +/- 14 spikes/s (68 +/- 23%) in hypertensive rabbits. Neither indomethacin nor prostacyclin (n = 5) influenced the pressure-diameter relation of the carotid sinus. The increase in prostacyclin (6-keto-PGF 1 alpha) formation by the sinus in response to its exposure to arachidonic acid (10 microM) was significant (P less than 0.05) in the normotensives (1,627 +/- 344%; n = 5) but not in the hypertensives (583 +/- 353%; n = 5). We conclude that the decreased baroreceptor activity in chronic hypertension may not be caused by decreased distensibility of the vascular wall of the sinus and that endogenous prostanoids that contribute to baroreceptor activation in normotensive rabbits fail to do so in hypertensive rabbits. This appears to be due to decreased formation of prostacyclin rather than decreased sensitivity of the baroreceptors to prostacyclin. The results suggest a new mechanism that contributes to chronic baroreceptor resetting in hypertension.
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PMID:Mechanism of decreased baroreceptor activity in chronic hypertensive rabbits. Role of endogenous prostanoids. 211 25

The purpose of this study was to clarify how the metabolism of vascular prostacyclin (PGI2) and thromboxane (TX) A2 in spontaneously hypertensive rats (SHR) is involved in aging and development of hypertension. We removed the aortic walls from 5-week-old and 20 to 25-week-old SHR and age-matched Wistar Kyoto rats (WKY). At 5 weeks of age, there was no significant difference in basal and maximal (arachidonic acid 0.1 mM) 6-keto-PGF1 alpha production between SHR and WKY, but the TXB2 generation in the SHR aortic wall was markedly enhanced as compared with that in WKY. At 20 to 25 weeks of age, the SHR aortic wall synthesized about 1.5 times more 6-keto-PGF1 alpha in the basal condition and twice as much as in the maximal condition as did the WKY wall. However there was no significant difference in TXB2 production between SHR and WKY. Age-dependent increase of vascular 6-keto-PGF1 alpha was greater in SHR than in WKY. Moreover, the maximal/basal 6-keto-PGF1 alpha production ratio increased with age in SHR, but not in WKY. The synthesis of vascular TXB2 was enhanced with age in WKY, but did not change with age in SHR. These data suggest that not only the enhanced basal generation of vascular 6-keto PGF1 alpha but also a much greater reservoir of 6-keto-PGF 1 alpha synthesis in SHR was induced by both hypertension and maturity. The increased production of vascular TXB2 in young SHR may affect the development of hypertension.
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PMID:Changes in vascular wall production of prostacyclin and thromboxane A2 in spontaneously hypertensive rats during maturation and the concomitant development of hypertension. 223 14

The effect of EPA enriched marine oil on platelet function in 12 cases of hypertension, 15 cases of diabetes and 20 cases of coronary heart disease is reported. The result of our study showed that there was platelet hyperfunction of various degrees in patients with those three kinds of diseases. The murine oil had an effect of inhibition, which were manifested by the prolongation on bleeding time, and decreased on platelet adhesion and aggregation. TxB2 in plasma was reduced, while 6-keto-PGF increased. There was no influence of EPA enriched fish oil on blood sugar and liver or kidney function. The authors concluded that platelet hyperfunction is an important element in the development of cardio vascular and cerebro vascular complications and increases the mortality rates in these diseases. Treatment with such a drug has beneficial effect with clinical improvement.
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PMID:[The effect of eicosapentaenoic acid enriched marine oil on the platelet function in hypercoagulable state]. 228 70

Vasodilator prostaglandins produced in the renal medulla have a role in blood pressure regulation, beyond modulation of sodium and water retention. Systemic vasodilation resulting from effects of renomedullary prostaglandins lowers systemic vascular resistance, and administration of NSAIDs elevates blood pressure in hypertensive patients treated with diuretics and/or beta blockers, in patients with myocardial infarction, and in patients taking sympathomimetic agents such as phenylpropanolamine. Aspirin, which appears in the urine as salicylic acid (which has no effect on cyclooxygenase) has not been implicated as a drug which attenuates blood pressure control. Similarly, sulindac, the active sulfide metabolite of which is not filtered, does not inhibit renal synthesis of prostaglandins, though given in doses sufficient to inhibit serum thromboxane and 6-keto PGF 1-alpha. In a double-blind complete crossover study of blood pressure and renal function in hypertensive patients controlled with timolol-hydrochlorothiazide, sulindac lowered blood pressure significantly, whereas naproxen and piroxicam significantly raised blood pressure, in the absence of any effect on GFR, plasma renin, weight, creatinine clearance, or urinary sodium. It is suggested that for arthritic patients with hypertension, the NSAIDs of choice are aspirin and sulindac.
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PMID:The arthritic patient with hypertension: selection of an NSAID. 354 Nov 67

We studied prostaglandins and kallikrein urinary excretion in 14 children with acute poststreptococcal glomerulonephritis within 48 hours of hospital admission (period A), and again, 4-6 weeks later, when they were clinically recovered (period B). Seventeen apparently healthy children were studied as controls. The results (mean +/- SEM) indicate that PGE2 urinary excretion (ng/kg/day) was diminished during both periods of study (control group = 2.06 +/- 0.43, patients = period A 0.91 +/- 0.28 [P less than 0.02], period B 0.92 +/- 0.21 [P less than 0.02]). PGF2 alpha urinary excretion (ng/kg/day) was also suppressed during period A, but not during period B when large individual variability existed (control group = 7.10 +/- 1.07, patients period A 3.56 +/- 0.66 [P less than 0.001], period B 10.51 +/- 5.01 [NS]). Kallikrein urinary excretion (EU/kg/day) was also depressed during the acute phase and remained low during convalescence (control group = 0.492 +/- 0.1, patients period A 0.143 +/- 0.044 [P less than 0.001], period B 0.265 +/- 0.093 [P less than 0.02]). There was no difference in PGE/PGF ratio between controls and patients in the periods of study (control 0.328 +/- 0.055, period A 0.395 +/- 0.144, period B 0.384 +/- 0.128). Urine volume (ml/day) was lower in period A (582 +/- 75.8) but comparable in period B (1020 +/- 140.2) and control children (1210 +/- 80.2). No correlation could be found between the urinary excretion of PGE2, PGF2 alpha and kallikrein with any of the following parameters: urinary or serum sodium and potassium, serum or urinary osmolality, Cosm, urine flow, plasma renin activity, plasma or urinary aldosterone, hypertension or fluid retention.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of prostaglandins (PGE2 and PGF2 alpha) and kallikrein in acute glomerulonephritis. 658 Sep 82

Experiments were carried out on salt-loaded rats (1.5% NaCl as drinking fluid) to further explore the mechanisms by which blood pressure increases after a linoleic acid-deficient (LAd) diet. In 4-week-old LAd rats (0.5 cal% LA, hydrogenated palm kernel fat) compared to linoleic acid-rich rats (LAr, 13.3 cal% LA, sunflower oil), we observed, from the base of a reduced content of omega-6-polyunsaturated fatty acids in the tissues, an increase in blood pressure by 12 mm Hg (p less than 0.001), a diminished formation of prostaglandin E (PGE), and an unchanged formation of PGF in the aorta as well as a reduction in the in vitro uptake of 14C-norepinephrine into cardiac, aortic, and renal tissues, and a reduced degradation rate of 14C-norepinephrine in cardiac tissue. These differences in LAr vs LAd rats were not exaggerated. With respect to aortic PGE formation, 14C-norepinephrine uptake into aortic and renal tissues and 14C-norepinephrine degradation even lessened when the diet was begun prenatally, although the reduction of omega 6-polyunsaturated fatty acids in the tissues was aggravated. Our conclusion is that a fault in catecholamine inactivation may be involved in the pathogenesis of increased sympathetic activity and blood pressure elevation in LAd-fed, salt-loaded rats, possibly via alterations of endogenous prostanoid formation.
Hypertension
PMID:Impaired catecholamine inactivation. A prohypertensive stimulus after dietary linoleate deficiency in salt-loaded rats? 658 Nov 24


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