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

It is possible to induce labour in pathological pregnancies after artificial ripening of the cervix. The present study concerns 70 patients (45 primipara, 25 multipara). The main pathologies are hypertension of pregnancy and pregnancies past dates. Prostaglandin F2 alpha has been used with a Tylose gel containing 5 mg of PGF2 alpha introduced by the extra-amniotic route. The cervical change was noted using Bishop's score. The mean increase of the cervical score was 0.8 with the first PGF2 alpha gel. The total mean increase was 1.2. Two cases of hyperstimulation of the uterus were observed and they led to Caesarean section. Prostaglandin gel induced labour in 56% of the patients. The mean time between the introduction of the gel and the delivery was 14 h for primipara and 10 h for multipara. Other patients were induced with oxytocin on the following day. Epidural analgesia was widely used in this study (in 64% of cases). The mean duration of labour was 6 h 10 for primipara and 4 h 30 for multipara. 30% of the patients needed Caesarean section but there was a marked difference between primipara (36%) and multipara (4%). After a review of the literature the authors conclude that it is useful to ripen the cervix prostaglandin but, as foreign authors do, they think that PGE2 should be more efficient.
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PMID:[Maturation of the cervix uteri using prostaglandin F2 alpha before induction of labor in pathologic pregnancies]. 657 95

The three main risk factors for cardiovascular disease, smoking, hypertension, and hyperlipidaemia, are examined in the light of changing world trends and the mechanisms by which they aggravate this large group of conditions. Prostaglandin activity within the vessel wall and the blood platelets may be disturbed by the risk factors, the control of which in programmes of primary prevention has been followed by striking reductions in cardiovascular morbidity and mortality in two of the world's worst-affected areas. Secondary preventive application of these same measures may improve the outcome in the treatment of established cardiovascular disease in the heart, brain, or limbs. Present advances in combined investigation and multifocal surgical treatment are described against a background of increasing safety throughout the perioperative period.
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PMID:The total care of the arteriosclerotic patient. 697 70

The present investigation demonstrates that chronic intrarenal PGE2 infusion results in a PRA-induced increase in arterial pressure. This conclusion is supported by an 8-fold rise in PRA and the marked reduction of arterial pressure during saralasin and CEI infusion. If the chronic effects of endogenously released PGE2 are similar to arterial administration, then the net effect of chronically elevated renal PGE2 in the dog appears to be a moderate, sustained hypertension.
Adv Prostaglandin Thromboxane Res 1980
PMID:Effect of chronic intrarenal prostaglandin E2 infusion and angiotensin II blockade on arterial pressure in the dog. 698 77

The effect of high salt intake on vascular and renomedullary prostaglandin (PG) synthesis was compared in Sprague-Dawley and salt-sensitive (S) and -resistant (R) Dahl rats. Animals were given a diet containing either 0.6% or 8% NaCl starting at 5 weeks of age, and were sacrificed 6 weeks later. Systolic blood pressure of S rats increased to 220 +/- 7 mm Hg but was unaffected in R and Sprague-Dawley rats. Prostaglandin synthesis was studied in aortic rings and renomedullary microsomes using 14C-arachidonate as substrate. [3H]PGE2 degradation was measured in the renocortical cytosol. In Sprague-Dawley and R rats, aortic PGI2 synthesis was not affected by high salt intake, while a significant increase compared to animals on 0.6% NaCl (from 608 +/- 84 to 992 +/-108 pmoles/60 min, p less than 0.05) was noted in S rats. Enhancement of PGI2 synthesis in S rats may be secondary to the hypertension. Salt-loading consistently stimulated renomedullary PGE2 synthesis in all three animal groups. S rats, however, had the lowest PG synthesis in renal medullas compared to Sprague-Dawley and R rats when placed on either diet. Thus, even after 6 weeks on high salt, S rats did not reach the levels of PGE2 synthesis seen in R or Sprague-Dawley rats on regular diet. The activity of cortical 15-hydroxyprostaglandin dehydrogenase was increased by salt-loading in S and Sprague-Dawley, but not in R rats. R rats had lower dehydrogenase activity than the other two groups when placed on either diet. The observed differences in PG synthesis and catabolism will tend to maintain the net output of renal PGs highest in R and lowest in S rats. These differences correlate with the reported differences in renal papillary flow between these two rat strains and may be relevant to their susceptibility or resistance to hypertension in response to salt.
Hypertension
PMID:Effect of salt on prostaglandin metabolism in hypertension-prone and -resistant Dahl rats. 721 76

It has recently been reported that synthesis of the vasodilatory prostaglandin, prostacyclin, is decreased in human pregnancy-induced hypertension (PIH). Prostaglandin production is regulated mainly by the enzyme phospholipase A2. We report here that serum levels of a potent phospholipase A2 inhibitor (gravidin) were elevated during early pregnancy in women who later developed PIH compared with those who remained normotensive throughout pregnancy. It is suggested that high circulating levels of this potent phospholipase inhibitor may account for the reported decrease in prostacyclin synthesis and contribute to the development of pregnancy-induced hypertension.
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PMID:Raised serum gravidin levels are associated with pregnancy-induced hypertension. 847 84

Cellular calcium modulates enzyme activity, cell proliferation, and differentiation. In vascular smooth muscle cells (VSMC), calcium may contribute to increased vascular contractility and structural alterations in both hypertension and atherosclerosis. We investigated the role of calcium in angiotensin II (AII)-induced prostaglandin release and DNA synthesis in VSMC. Prostaglandin levels were determined by radioimmunoassay, and DNA synthesis was determined by the incorporation of [3H]thymidine. AII dose-dependently stimulated the release of prostaglandin E2 and prostaglandin I2, and this effect was synergistically enhanced by the Ca2+ ionophore A23187. Conversely, the AII response was inhibited by EGTA, a chelator of Ca2+ ions and by verapamil and nifedipine, two Ca2+ channel blockers or by incubation of the cells without exogenous Ca2+. TMB-8, an inhibitor of calcium mobilization, also strongly reduced angiotensin response. Similar results were obtained for angiotensin III (AIII) and vasopressin, two other agonists of prostaglandin production. AII- or serum-stimulated DNA synthesis was almost abolished by EGTA, whereas TMB-8, verapamil, and nifedipine had little or no effect. The production of prostaglandins triggered by angiotensins and vasopressin in VSMC is dependent on both intracellular and extracellular calcium, with calcium entering through L-type Ca2+ channels. Extracellular calcium is important for AII and serum mitogenic activity, but L-type Ca2+ channels do not appear to be implicated.
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PMID:Role of calcium in angiotensin II-induced prostaglandin release and DNA synthesis in rat vascular smooth muscle cells. 872 Apr 17

Prostaglandin concentrations are elevated in intestinal lymph during brief abdominal visceral ischemia, and exogenously applied prostaglandins can directly stimulate or sensitize ischemically sensitive visceral sympathetic nerve fibers. However, it is not known if prostaglandin production during abdominal ischemia is sufficient to contribute to the reflex cardiovascular response (e.g., hypertension). Accordingly, in anesthetized cats, the femoral artery was cannulated for measurement of arterial blood pressure, and the superior mesenteric and celiac arteries were isolated and fitted with snare occluders. After dual occlusion of these arteries (</=20 min), the cyclooxygenase inhibitors indomethacin (10-20 mg/kg iv, n = 5, group 1) or acetylsalicylic acid [50 mg/kg iv (n = 6) and ia (n = 2); group 2] were administered and ischemia was repeated. In group 1, indomethacin lowered the reflex arterial blood pressure increment by 39% from 31 +/- 7 to 19 +/- 5 mmHg (P > 0.05). In group 2, acetylsalicylic acid significantly (P < 0.05) reduced the reflex rise in blood pressure by 46% (28 +/- 3 to 15 +/- 4 mmHg). A second, more invasive preparation (group 3) was utilized to 1) minimize the confounding, transient, nonreflex rise in blood pressure associated with arterial ligation, and 2) further assess the inhibitory effect of indomethacin. In group 3, the ischemia-induced blood pressure rise of 28 +/- 6 mmHg was reduced by 43% to 16 +/- 4 mmHg after indomethacin (n = 4, P < 0.05). Thus blockade of the cyclooxygenase pathway by two structurally dissimilar inhibitors attenuated the visceral-cardiovascular reflex response to brief ischemia, suggesting that prostaglandins released during visceral ischemia contribute significantly to the activation of the reflex cardiovascular response.
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PMID:Reflex cardiovascular response to brief abdominal visceral ischemia is mediated in part by prostaglandins. 1056 32

Stretching of the renal pelvic wall activates renal mechanosensitive neurons, resulting in an increase in afferent renal nerve activity (ARNA). Prostaglandin (PG)E(2) plays a crucial role in the activation of renal mechanosensitive neurons through facilitation of the release of substance P from the sensory neurons in the renal pelvic wall. Because wall stretch may induce cyclooxygenase-2 activity, we examined whether cyclooxygenase-2 was expressed in the renal pelvic wall and whether activation of cyclooxygenase-2 contributed to the ARNA response produced through increased renal pelvic pressure. In situ hybridization showed a strong cyclooxygenase-2 mRNA signal in the papilla and subepithelial layer of the renal pelvic wall from time control kidneys and from kidneys exposed to 15 minutes of increased renal pelvic pressure in anesthetized surgically operated rats. In anesthetized rats, an increase in renal pelvic pressure increased ARNA by 40+/-2% and increased renal pelvic release of PGE(2) from 289+/-46 to 1379+/-182 pg/min (P<0.01). Renal pelvic perfusion with the cyclooxygenase-2 inhibitor etodolac reduced the increases in ARNA and PGE(2) by 66+/-7% and 55+/-13%, respectively (P<0.01). Likewise, the cyclooxygenase-2 inhibitor 5, 5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone reduced the increases in ARNA and PGE(2) by 43+/-5% and 47+/-8%, respectively. We conclude that cyclooxygenase-2 is expressed in the renal pelvic wall and that the activation of cyclooxygenase-2 contributes to the stimulation of renal mechanosensitive neurons in the pelvic wall.
Hypertension 2000 Jan
PMID:Cyclooxygenase-2 involved in stimulation of renal mechanosensitive neurons. 1064 27

Differences between prostaglandins I(2) and E(2) in their renal synthesis and pathophysiological roles were investigated in unilateral renovascular hypertension of different severities in 18 patients: 6 with mild stenosis (<75% of the diameter) of the renal artery, 7 with moderate stenosis (75% to 90%), and 5 with severe stenosis (>90%). Before and after aspirin administration (10 mg/kg), renal venous and aortic plasma was assayed for 6-ketoprostaglandin F(1alpha) (instead of prostaglandin I(2)), prostaglandin E(2), and renin activity. In mild or moderate stenosis, the mean 6-ketoprostaglandin F(1alpha) level in renal venous plasma from the stenotic side was not different from that from the normal side or from aortic plasma. Prostaglandin E(2) levels and renin activity in such patients were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited prostaglandin E(2) synthesis and suppressed renin release from stenotic kidneys and lowered blood pressure as the renin activity decreased in patients with mild or moderate stenosis. In severe stenosis, levels of 6-ketoprostaglandin F(1alpha) and prostaglandin E(2) were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited the synthesis of both prostaglandins and suppressed renin release from the stenotic kidney. In patients with unilateral renovascular hypertension with mild or moderate stenosis of the renal artery, prostaglandin E(2), rather than I(2), seems to contribute to further acceleration of renin release. Prostaglandin I(2) may increase and participate in further renin release when the stenosis is severe.
Hypertension 2001 Jul
PMID:Prostaglandin I(2)/E(2) ratios in unilateral renovascular hypertension of different severities. 1146 55

Prostaglandin H synthase (PGHS) is a rate-limiting enzyme in the production of prostaglandins and thromboxane, which are important regulators of vascular function. Under normal physiological conditions, PGHS-dependent vasodilators (such as prostacyclin) modulate vascular tone. However, PGHS-dependent vasoconstriction (mediated by thromboxane and/or its immediate precursor, PGH(2)) predominates in some vascular pathologies (eg, systemic hypertension, diabetes, cerebral ischemia, and aging). This review will discuss the role of PGHS-dependent modulation of vascular function in a number of vascular beds (systemic, pulmonary, cerebral, and uterine) with an emphasis on vascular pathophysiology. Moreover, the specific contributions of the different isoforms (PGHS-1 and PGHS-2) are discussed. Understanding the role of PGHS in vascular function is of particular importance because they are the targets of the commonly used nonsteroidal antiinflammatory drugs (NSAIDs), which include aspirin and ibuprofen. Importantly, with the advent of specific PGHS-2 inhibitors for treatment of conditions such as chronic inflammatory disease, it is an opportune time to review the data regarding PGHS-dependent modulation of vascular function.
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PMID:Prostaglandin H synthase and vascular function. 1159 87


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