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

The effects of 5 days low sodium diet and diuretic were studied in 7 normotensive acromegalics, 8 hypertensive acromegalics and 12 normal subjects. Plasma renin activity was significantly lower in both groups acromegalics, compared with that of normal subjects. Plasma aldosterone was similar in normotensive acromegalics and healthy controls. The hypertensive acromegalics showed increased plasma aldosterone levels and blunted responses of plasma renin activity and plasma aldosterone to sodium depletion. Urinary prostaglandin E2 was significantly lower in hypertensive acromegalics before and after sodium depletion in comparison with normal subjects. Urinary 6-keto prostaglandin F1 alpha and thromboxane B2 were similar in all groups studied. The decreased production of PGE2 could contribute to the development of arterial hypertension in actomegaly.
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PMID:Effect of sodium depletion on the renin-angiotensin-aldosterone system and renal prostaglandins in acromegalic patients. 209 66

Prostaglandin (PG) E2 receptor-adenylate cyclase system was studied in the kidney of 12-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to evaluate the role of this system in hypertension. PGE2 receptors were determined by a radioligand binding method using [3H]-PGE2. Adenylate cyclase responses to PGE2, sodium fluoride (NaF) and forskolin were also measured. The concentration of PGE2 receptor was increased in SHR compared with WKY. PGE2- and NaF-stimulated adenylate cyclase activities were significantly lower in SHR than WKY. There was no significant difference in forskolin-stimulated adenylate cyclase activity between SHR and WKY. NaF activates the nucleotide binding regulatory protein (G-protein) and forskolin directly activates the catalytic unit. These results indicate that the activity of G-protein coupled with renal PGE2 receptors is deficient in SHR. This defect may contribute to the elevation of blood pressure, through sodium retention.
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PMID:Deficient activity of nucleotide binding regulatory protein coupled with PGE2 receptor in renal medulla of spontaneously hypertensive rats. 210 7

Endothelium-dependent contractions to acetylcholine and endothelium-independent contractions to oxygen-derived free radicals in the aorta of the spontaneously hypertensive rat (SHR) are mediated by an unidentified product of the cyclooxygenase pathway of arachidonic acid metabolism. To determine the role of thromboxane A2 (TXA2) or prostaglandin H2 (PGH2) in these contractions, rings of the thoracic aorta of SHR were suspended in organ chambers for measurement of isometric force. Acetylcholine caused endothelium-dependent contractions in quiescent rings from SHR aortas. Oxygen-derived free radicals generated with xanthine plus xanthine oxidase caused contractions in rings without endothelium. Dazoxiben (thromboxane synthetase inhibitor) did not affect contractions evoked by acetylcholine. AH 23,848, SQ 29,548, or R 68,070 (TXA2/PGH2 receptor antagonists) inhibited contractions to U 46,619 (a TXA2/PGH2 receptor agonist), acetylcholine, and oxygen-derived free radicals. Acetylcholine stimulated the release of prostacyclin from Wistar-Kyoto (WKY) rat and SHR aortas but not the release of other prostaglandins (PGE2, PGF2 alpha, TXA2). Oxygen-derived free radicals did not stimulate the release of prostaglandins from either SHR or WKY rat aortas. These results demonstrate that stimulation of TXA2/PGH2 receptors probably by PGH2 might be involved in endothelium-dependent contractions. Oxygen-derived free radicals, which might be an endothelium-derived contracting factor or factors, ultimately cause contraction by stimulation of TXA2/PGH2 receptors.
Hypertension 1990 Jun
PMID:Thromboxane A2 receptor antagonists inhibit endothelium-dependent contractions. 214 Oct 3

Renal neurotransmission and its modulation by prostaglandin (PG) E2 (0.06 microM) and indomethacin (10 microM) was investigated in isolated kidneys of adult spontaneously hypertensive (SHR) and normotensive control (WKY) rats. After preincubation with [3H]-noradrenaline the renal nerves were stimulated. The stimulation induced (S-I) outflow of radioactivity was taken as an index of noradrenaline release. The S-I outflow of radioactivity from SHR and WKY kidneys was similar but S-I pressor responses were enhanced in kidneys of SHR. PGE2 inhibited and indomethacin enhanced the S-I outflow of radioactivity in kidneys of WKY and SHR to a similar extent. This inhibitory effect of PGE2 is due to activation of inhibitory prejunctional PGE2 receptors. Neuronally released noradrenaline stimulates a local formation of PGE2 which then transjunctionally inhibits noradrenaline release. Renal noradrenaline release in the adult SHR and its modulation by PGs is not altered. An enhanced postjunctional responsiveness of the renal vasculature may contribute to the maintenance of hypertension in the adult SHR.
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PMID:Prostaglandin E2 inhibits and indomethacin enhances noradrenaline release in isolated kidneys of adult spontaneously hypertensive rats. 226 6

With radioimmunoassay, daily urinary levels of prostaglandins E2 and F2 alpha (PGE2, FGF2 alpha were measured in 45 patients with hypertensive disease, 13 patients with chronic diffuse glomerulonephritis and 14 healthy persons. A progressive reduction in urinary PGE2 excretion was found to accompany the occurrence of labile arterial hypertension (AH), its stabilization, and development of malignant AH in patients with hypertensive disease or chronic diffuse glomerulonephritis. When labile AH developed, urinary PGF2 alpha excretion was increased, but when AH stabilized, its excretion became increased up to the baseline level. The specific features of malignant AH are significantly higher urinary PGF2 alpha and sharply greater PGF2 alpha/PGE2 coefficient. The identified abnormal metabolism of renal prostaglandins may contribute to the stabilization of blood pressure at a high level and to the development of malignant AH.
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PMID:[Urinary prostaglandin levels in patients with arterial hypertension with benign and malignant course]. 233 58

The authors induced 105 deliveries by extraamniotic administration of PGE2 (prostin Upjohn). The initial dose was 1-2 tablets, depending on the maturity of the portio uteri. If the contractions did not start within two hours, the dose was repeated. The sac was disrupted when the contractions were regular and the os uteri was larger than 2 cm. If necessary uterine activity was stimulated by small doses of Oxytocin (in 29%). Indication for induction was a programmed delivery (44.7%), protraced pregnancy (31.5%), diabetes mellitus (10.5%), a period of more than 24 hours after drainage of amniotic fluid without contractions (5.7%), hypertension or renal disease during gestation (4.8%) and hypotrophy of the foetus (2.8%). Inductions were successful in 96.2% of the patients. The parity of the patients influenced the interval between the onset of induction and the onset of uterine contractions, the duration of the first and second stage of labour and the consumption of Prostin tablets. The age of the patient, occupation, obesity and operation on the uterus did not affect the success of induction. There were no serious pathological findings during the third stage of labour, nor serious side-effects. The condition of the neonates was satisfactory.
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PMID:[Labor induction using extra-amniotic administration of PGE2]. 235 Jul 87

A group of 89 apparently healthy subjects and 175 patients with essential hypertension (EH) and systolic (atherosclerotic) hypertension aged 25 to 74 years were surveyed. The healthy subjects were found to have changes in prostaglandin (PG) synthesis and metabolism: a reduction in blood plasma concentration of PGE2 and its urinary excretion, a rise in plasma PGF2 level, and, generally, increase in the pressor and decrease in depressor potentials of the PG system. In the EH patients, changes in the PG synthesis and metabolism were unidirectional and had quantitative variations. The differences in the PG levels of healthy and EH-afflicted individuals were found to become less marked with age. The patients with systolic hypertension exhibited higher plasma prostacyclin concentrations as compared to the age-matching control, which is evidence of a lower pressor potential of the PG system than that of the EH patients. The nature and magnitude of changes in the PG system play a certain role in blood pressure formation and in development of the hemodynamic variant of arterial hypertension.
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PMID:[Age-related characteristics of the prostaglandin system in healthy subjects and in patients with arterial hypertension: hypertonic disease and systolic (atherosclerotic) hypertension]. 235 36

Evidence in vitro and in humans suggest that Mg2+ can alter systemic and renal vascular tone. However, the mechanism of these effects is not known. The role of vasodilator prostaglandin release and Ca2+ flux in Mg2+-induced changes in blood pressure and renal blood flow was studied in 10 normal subjects maintained on a fixed 80-mEq Na+ and K+ diet. Magnesium sulfate infused at 200 mg/hr for 3 hours reduced systolic and diastolic blood pressure within 1 hour (from 119 +/- 2 [SEM] to 109 +/- 4 mm Hg systolic; from 74 +/- 3 to 64 +/- 4 mm Hg diastolic; p less than 0.02). This hypotensive response was seen in all subjects and persisted for 3 hours. The pulse rate did not change, but renal blood flow (p-aminohippurate clearance) increased (from 902 +/- 78 to 1108 +/- 130 ml/min/1.73 m2; p less than 0.05). The Mg2+ infusion produced a significant increase in the excretion of the stable prostaglandin I2 (PGI2) metabolite 6-keto-PGF1 alpha (from 96 +/- 12 to 154 +/- 16 ng/g creatinine; p less than 0.01). In contrast, urinary PGE2 was not altered (328 +/- 75 vs 399 +/- 145 ng/g creatinine; p greater than 0.6). To evaluate the functional role of PGI2 release, the cyclooxygenase inhibitors indomethacin (75 mg) or ibuprofen (600 mg) were given before the Mg2+ infusion. Both cyclooxygenase blockers, given in doses that inhibited immunoreactive 6-keto-PGF1 alpha release, completely prevented the Mg2+-induced decline in blood pressure and increased renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Apr
PMID:Evidence that prostacyclin mediates the vascular action of magnesium in humans. 243 56

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the capacity of PGE2 synthesis in cultured renal papillary collecting tubule cells from young (4-week-old) and aged (16-week-old) SHR and control Wistar-Kyoto rats (WKY). Basal levels of PGE2 synthesis were lower in young SHR cells than in WKY cells (p less than 0.001). Arachidonic acid-stimulated PGE2 synthesis, however, had a slight tendency to be higher in SHR cells than in WKY cells. Bradykinin- and A23187-stimulated PGE2 synthesis were similar in both strains. Basal levels of cyclic AMP were also lower in young SHR cells than in WKY cells (p less than 0.001), but the cAMP response to exogenous PGE2 was equal between the strains. In papillary collecting tubule cells from aged rats, basal levels of PGE2 and cyclic AMP as corrected for cellular protein were significantly lower than those in young rats, but there was no difference between the strains. Urinary excretion of PGE2 and thromboxane B2 was equal in aged SHR and WKY. These results suggest that papillary collecting tubule of young SHR and WKY may differ in the metabolism of PGE2 and cyclic AMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.
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PMID:PGE2 synthesis in cultured renal papillary collecting tubule cells from young and aged spontaneously hypertensive rats. 248 50

Prostaglandin (PG) I2 and PGE2 are known to stimulate left ventricular receptors with nonmyelinated vagal afferents. The present experiments were performed to determine the effects of intracoronary infusion of PGE2 (10-50 ng.kg-1.min-1) and arachidonic acid (50-100 micrograms.kg-1.min-1) on the baroreflex control of heart rate in conscious dogs. Dogs were anesthetized with pentobarbital sodium and were instrumented using sterile surgical techniques. After recovery, baroreflex pressure-heart rate curves were constructed by varying arterial pressure with partial occlusions of the descending aorta or inferior vena cava. Intracoronary infusion of PGE2 significantly inhibited the maximum heart rate achieved during unloading of baroreceptors, attenuated the heart rate range, and decreased the maximum slope of the baroreflex curve; PGE2 had no significant effect on the minimum heart rate during hypertension. Intravenous infusion of PGE2 did not cause significant baroreflex inhibition, and pericoronary nerve block in three dogs prevented the effects of intracoronary PGE2. Intracoronary infusion of arachidonic acid had effects on the baroreflex control of heart rate similar to those of PGE2. The effects of arachidonic acid infusion were prevented by cyclooxygenase blockade. Thus intracoronary PGE2 and arachidonic acid inhibit the baroreflex control of heart rate most likely via stimulation of left ventricular receptors with vagal C-fiber afferents. The effects of arachidonic acid were secondary to synthesis of prostaglandins.
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PMID:PGE2 and arachidonate inhibit the baroreflex in conscious dogs via cardiac receptors. 249 39


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