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

Prostaglandin E2 gel is a useful agent for ripening and dilating the cervix. Since it is not available in the US, it must be prepared by thawing and grinding a 20 mg prostaglandin E2 suppository, mixing in a small amount of methylcelulose gel, and blending. The resulting gel is stored frozen in a 3 ml plastic syringe. The gel may be administered intracervically, intravaginally, or extraamniotically. Cervical administration of .5 mg prostaglandin E2 in 2-3 ml of viscous gel is most popular, but intravaginal administration is easiest, although it requires a higher dose (1-5 mg prostaglandin E2 in 2-10 ml of gel). The condition of the cervix is usually favorable for labor induction within 12 hours (range 4-24 hours). 59 clinical trials were conducted among 3313 pregnancies. In patients with unfavorable cervix induction of labor was successful in 83% of those treated with the gel but in only 53% of untreated patients. In women with an unfavorable cervix the gel is more effective if administered intracervically. In patients with favorable cervix, 66% of nulliparas and 82% of multiparas were delivered without oxytocin. Prostaglandin E2 gel has been used successfully even in women with prolonged pregnancy, hypertension, ruptured membranes, and fetal death. It can also be used to induce late 1st trimester abortion. Side effects of the gel are mild and minor. Prostaglandin E2 gel has thus been shown to effect cervical ripening and dilatation, reduce induction failures, shorten the induction-delivery interval, reduce oxytocin use, and lower the need for cesarean sections. Prefabricated prostaglandin E2 delivery systems should be approved by the Food and Drug Administration for commercial use.
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PMID:Prostaglandin E2 gel for cervical ripening and induction of labor: a critical analysis. 264 30

To assess the participation of cardiovascular eicosanoids (prostaglandins and thromboxanes) system in the initiation of genetic hypertension, we examined eicosanoids metabolism in the heart, aortic wall and kidney in prehypertensive and hypertensive rat models for spontaneous hypertension (SHR). Vasoconstrictor thromboxane A2 (TXA2) generation in the aortic wall was significantly enhanced by 49% in the prehypertensive and by 18% in the hypertensive SHR when compared to the respective normotensive Wistar-Kyoto rats. Cardiac TXA2 content was significantly increased as well by 14% in the prehypertensive and by 30% in the hypertensive SHR. Moreover, vascular vasodepressor eicosanoids generation was decreased by 10% for PGI2 and by 29% for PGD2 in the prehypertensive SHR although the alterations were eliminated in the hypertensive SHR. In contrast to the cardiovascular eicosanoids system, there was no difference in renocortical TXA2 content in either young or adult SHR while vasodepressor prostaglandins contents were decreased by 29% for PGE2 and by 33% for PGD2 in SHR when they were in the prehypertensive stage. Thus, in the prehypertensive stage of SHR, the cardiovascular eicosanoids system exhibited enhanced vasoconstrictor TXA2 and decreased vasodepressor prostaglandins, thereby producing a vasoconstrictor state. These data indicate that the alterations in the cardiovascular eicosanoids system partially contribute to the initiation of hypertension in SHR.
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PMID:Alterations of the cardiovascular and renal prostaglandins and thromboxanes system in prehypertensive spontaneously hypertensive rats. 266 86

Injection of PGF2alpha intratubally, with other conservative management, was compared in 30 consecutive women with proven ectopic pregnancy, to 100 prior women treated surgically. The patient group were all 45 admitted after November 1987 to University of Vienna Hospital with suspected ectopic pregnancy, later proven in 30 by history, positive hCG, ultrasound and laparoscopy; the controls were 74 confirmed cases out of 101 suspected ectopic pregnancies admitted from January 1986- October 1987. They were treated with 5 or 10 mg PGF2alpha (Miniprostin F2alpha, Upjohn, Vienna), injected transabdominally with a 17-gauge needle, during laparoscopic visualization. In 6 patients, 2-3 mg Pgf2alpha was injected into the corpus luteum, but this practice was discontinued when 3 developed tachycardia, hypertension and extrasystole. 25 mg estrogen was injected into the ovary as a luteolytic subsequently. Most women also received PGE2 (Sulprostone, Schering, Berlin) twice daily im, although 4 could not tolerate side effects of nausea and vomiting. All women had hCG levels daily. 5 were treated by laparotomy because of rising hCG or clinical indications. In the control group 74 (73.3%) had laparotomy, and of these, 39 had total or partial salpingectomy, and 21 salpingotomy. Hysterosalpingography demonstrated tubal patency in 11 of 12 PG treated women tested to date; in contract, of 14 of the controls tested, none had patent tubes. 4 of the PG group have since conceived and delivered term infants. The benefits of this conservative method of treating ectopic pregnancy are apparent in the reduced morbidity, shorter hospital stay, simpler treatment technique, lower costs, and especially the higher rate of subsequent tubal patency and fertility.
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PMID:Prostaglandin injection for termination of tubal pregnancy: preliminary results. 271 7

We designed experiments to reveal the effects of a S2 serotonergic receptor antagonist, ketanserin, on the vascular eicosanoid system and the relevance to medial hyperplasia in spontaneously hypertensive rats (SHR). 2-week ketanserin treatment (5 mg/kg/day) significantly decreased systolic blood pressure by 7% when compared to untreated SHR. The blood pressure reduction was associated with a significant decrease in vascular thromboxane A2 (TXA2) generation and sustained prostacyclin (PGI2) production, thereby shifting PGI2/TXA2 ratio toward vasodilatation. In contrast, the trichlormethiazide treatment, which achieved blood pressure reduction to almost the same extent, significantly decreased PGI2/TXA2 ratio. Vasodilator eicosanoids, e. g. PGI2, PGE2 and PGD2, dose-dependently decreased (3H)-thymidine uptake by vascular smooth muscle cells in culture whereas vasoconstrictor TXA2 enhanced (3H) thymidine uptake in a dose dependent manner. Indeed 2 x 10(-5) M ketanserin significantly decreased (3H) thymidine uptake by vascular smooth muscle cells by 48% although the same dose of methysergide, nonspecific serotonin inhibitor, did not affect the uptake by vascular smooth muscle cells. These results clearly indicate that the blood pressure reduction in ketanserin treatment is uniquely associated with a decrease in vascular thromboxane generation, and that it is possibly beneficial to protect vascular wall against medial hyperplasia of vascular smooth muscle cells, an integral component of arterial sclerotic changes in hypertension.
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PMID:[The effects of ketanserin on vascular eicosanoid system in spontaneously hypertensive rats and their implications]. 274 98

The ability of angiotensin II and arachidonic acid to release immunoreactive prostaglandins into venous and ureteral effluents of rabbit isolated perfused kidneys was examined 7 days after suprarenal aortic coarctation (SRAC) or sham operation (SHAM). Renal vascular responses to angiotensin II were significantly enhanced in SRAC and accompanied by an enhanced venous efflux of bioassayable prostaglandins. Angiotension II-induced release of immunoreactive PGE2, PGF2 alpha, 6-keto PGF1 alpha and TxB2 into the venous effluent was exaggerated in SRAC. As angiotensin II did not stimulate TxB2 efflux in the SHAM group the induction of TxB2 release by SRAC is particularly noteworthy. These changes in eicosanoid release in response to angiotensin II were not mimicked by arachidonic acid administration. These results suggest that in renovascular hypertension angiotensin II-induced prostaglandin release is primarily augmented in the vascular compartment and is consistent with the sensitivity of renal function to cyclooxygenase inhibitors in renovascular hypertension.
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PMID:Exaggerated renal thromboxane and prostaglandin release by angiotensin II in suprarenal aortic coarctation hypertension. 274 7

The results of the study of depressor (PGE+A) and pressor (PGF2 alpha) prostaglandins in the blood plasma and of PGE2 and PGF2 alpha excretion in the urine of 52 patients with an acute stage of Itsenko-Cushing disease are presented. It has been established that the different components of the PG system have dissimilar changes: the absence of differences in the content of depressor and significant increase in pressor PG, which may be the cause of hypertension in Itsenko-Cushing disease. Stress due to insulin hypoglycemia and furosemide load brought about disturbances in the reaction of the PG system, which were more pronounced in the system pressor component. Disturbances of the PG system which were more pronounced in the presence of stable hypertension were established in all patients.
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PMID:[Prostaglandins in Itsenko-Cushing syndrome]. 277 63

The patients suffering from hypertonic nephritis were examined for renal hemodynamics, the activity of the renin-angiotensin-aldosterone system (RAAS), excretion of PGE2 and PGF2 alpha, and for a number of the parameters of water-electrolyte homeostasis. In A series, the patients suffering from latent and hypertonic nephritis (n = 11 in each group) were compared. In B series, two groups of the patients (n = 13 in each group) suffering from hypertonic nephritis associated with moderate or grave arterial hypertension were compared. The patients under comparison belonging to A and B series did not differ as regards the sex, age, nephritis standing, serum creatinine or proteinuria. As compared with the patients suffering from latent nephritis (A series), the patients with hypertonic nephritis showed a lower effective renal plasma flow, a greater resistance of the renal vessels, lesser PGE2 secretion, and a higher serum sodium concentration. As compared with the patients suffering from moderate hypertension (B series), the patients with associated hypertonic nephritis and grave hypertension demonstrated a higher resistance of the renal vessels, a higher activity of plasma renin, a larger concentration of plasma aldosterone and its excretion with urine, as well as a greater volume of the circulating blood. It is assumed that the development of arterial hypertension associated with hypertonic nephritis may be caused by renal hemodynamics deterioration, by relative activation of the renin-angiotensin system, inhibition of the depressor prostaglandin system and sodium retention. The progression of hypertension may be related to further deterioration of renal hemodynamics attended by RAAS activation and hypervolemia.
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PMID:[Mechanisms of the development of arterial hypertension in hypertonic nephritis]. 279 11

Differential-diagnosis tests for low-renin hypertension viz essential hypertension and arterial hypertension due to Conn's syndrome (adrenocortical adenoma or hyperplasia) have been assessed. The examined patients showed considerable humoral and metabolic differences, as compared to patients with high and normal plasma renin activity (PRA). For example, patients with essential hypertension and low PRA showed depressed noradrenalin and PGE2 secretion, increased PGF2 alpha secretion, low triglyceride level, and elevated erythrocyte sodium content. Patients with adrenocortical adenoma exhibited increased secretion of adrenalin, dopamine and PGF2 alpha, and a higher erythrocyte sodium level. Enhanced dopamine synthesis in patients with Conn's syndrome may be an adaptive response to a high aldosterone level.
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PMID:[Activity of the sympathetic nervous system and the levels of prostaglandins and intracellular electrolytes in patients with arterial hypertension and low plasma renin activity]. 307 43

The effects of glucocorticoid agonists RU 26988 (G) and dexamethasone (D) and antagonist RU 486 (AG) on aortic and renal prostaglandin (PG) production were studied in Wistar rats. Blood pressure increased in rats administered G (20 mg X kg-1 X day-1) during 1 or 3 days; such increase was prevented by AG (100 mg X kg-1 X day-1). Renal papillary PGE2 release was increased after a 3-day administration of G, and this was prevented by AG. Neither G nor AG altered basal 6-keto-PGF1 alpha aortic production. However, G inhibited and AG magnified the stimulatory effect of ionophore A 23187, added in vitro, on 6-keto-PGF1 alpha production; AG reversed G inhibition. In addition, AG alone (20 mg X kg-1 X day-1 X 3 days) enhanced the stimulatory effect of angiotensin II (10(-8) M), added in vitro, on 6-keto-PGF1 alpha release. In vitro studies were performed on renomedullary interstitial cells grown in culture; G and D depressed PGE2 production in a dose-dependent manner; AG at equimolar 10(-8) M concentration inhibited this effect. In conclusion, AG inhibits the effects of G on blood pressure and PG synthesis. G exerts strong depressor activity on in vitro PGE2 renal production, whereas in vivo effects are more complex. Endogenous G inhibits aortic prostacyclin production, an action unmasked by AG administration. Diminished stimulation of vascular prostacyclin synthesis may contribute to vascular hyperreactivity in G-induced hypertension.
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PMID:Effects of gluco- and antiglucocorticoids on renal and aortic prostaglandin synthesis. 309 51

In spontaneously hypertensive rats (SHR) between the ages of 6 and 8 weeks before the development of established hypertension, repeated daily subcutaneous administration of indomethacin, an inhibitor of cyclo-oxygenase, at a dose of 5 mg/kg/day enhanced significantly the development of spontaneous hypertension, but repeated daily subcutaneous administration of OKY 046, an inhibitor of thromboxane (TX)A2 synthetase, at a dose of 12 mg/kg/day did not alter the development of spontaneous hypertension. In SHR between the ages of 15 and 18 weeks with established hypertension, indomethacin or OKY 046 did not alter the high blood pressure as compared with the injection of vehicle. In both young and adult SHR, indomethacin decreased significantly urinary prostaglandin (PG)E2 and TXB2 excretion but not PGE2. These results indicate that cyclo-oxygenase products other than TXA2 may play a protecting role in the development of spontaneous hypertension in the rat whereas their contribution to the maintenance of hypertension may be unlikely. In addition, it is suggested that TXA2 may not be involved in the development and maintenance of spontaneous hypertension in the rat.
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PMID:Role of the prostaglandin-thromboxane system in the development and maintenance of spontaneous hypertension in the rat. 312 54


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