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

A rat model combining two-kidney, one-clip (2K1C) renovascular hypertension and streptozotocin-induced diabetes mellitus was used to assess the pathogenetic significance of vasodilator prostaglandins in diabetic glomerular injury. Glomeruli isolated from normotensive diabetic rats produced greater than normal amounts of PGE2 and 6-keto PGF1 alpha under in vitro incubation conditions. In 2K1C hypertensive-diabetic rats, glomeruli from unclipped kidneys (which are prone to accelerated diabetic glomerular injury) produced similarly elevated amounts of PGE2 and 6-keto PGF1 alpha, which significantly exceeded the levels produced by glomeruli from clipped kidneys (which are relatively protected from glomerular injury), despite exposure to a similar diabetic environment. In contrast, glomeruli from both unclipped and clipped kidneys of 2K1C hypertensive-non-diabetic rats produced normal amounts of PGE2 and 6-keto PGF1 alpha. These results suggests a correlation between vasodilator prostaglandin metabolism and susceptibility to diabetic glomerular injury, and illustrate that enhanced glomerular prostaglandin production is not an invariable metabolic consequence of hyperglycemia or insulin deficiency. The data also demonstrate that hemodynamic as well as metabolic factors may influence glomerular prostaglandin metabolism in experimental diabetes mellitus.
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PMID:Glomerular prostaglandin production in diabetic rats with renovascular hypertension. 316 82

Intravenous injection of prostaglandin (PG) E2 (0.01-1.0 mg/kg) induced a dose-dependent increase in the rectal temperature of urethane-anesthetized rats; the maximum change attained was 0.14 +/- 0.08 to 1.38 +/- 0.16 degrees C at 23 to 51 min after injection. The i.v. injection of PGE2 methyl ester (PGE2-Me), a lipophilic derivative of PGE2, resulted in hyperthermia 1.5-fold higher than that by PGE2 injection over the same dose range. The hyperthermia was associated with tachycardia, hypertension, cutaneous vasodilation and a rise in abdominal skin temperature. Using [3H]PGE2 and radioimmunoassay, we showed PGE2 to be transported into the brain immediately (15 sec) after the i.v. injection of the PG; the PGE2 content ranged from 2.3 +/- 0.5 to 102.6 +/- 5.5 ng/g of brain when given at 0.01 to 1.0 mg/kg, which was 0.07 to 0.13% of the administered dose. When [3H]PGE2-Me was used, the radioactivity in the brain at 15 sec after injection was 1.3- to 2.9-fold higher than that after [3H]PGE2 injection. However, 80% or more of PGE2-Me was hydrolyzed rapidly and recovered as PGE2 in the brain within 15 sec post-injection. PGE2-Me disappeared within 5 min. When PGE2 or PGE2-Me administered i.v. was followed in terms of PGE2, it decreased gradually in the brain with a half-life of 9.0 to 9.5 min in both cases, and was almost undetectable (less than 0.7 ng/g of brain) at the time when rectal temperature reached a peak. The maximum change and duration of hyperthermia were correlated closely with the PGE2 content in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central action of prostaglandin E2 and its methyl ester in the induction of hyperthermia after their systemic administration in urethane-anesthetized rats. 318 62

Renal arterial embolization and subsequent nephrectomy or nephrectomy alone were performed in 34 patients with renal cell carcinoma. Renal arterial embolization caused a blood pressure elevation concomitant with an increase in plasma renin activity (PRA), urinary aldosterone excretion or urinary prostaglandin (PGE2) excretion. Subsequent nephrectomy normalized hypertension and reduced the levels of these vasoactive substances. There were significant relationships between the increase in mean blood pressure and the increase in PRA, the increment in mean blood pressure and the increment in urinary aldosterone excretion, and the increase in PRA and increase in log urinary PGE2 excretion following embolization. These evidences suggest that enhancement of the renin-angiotensin-aldosterone system participates in the development of hypertension following embolization, and increased PRA may play an important role in the release of urinary PGE2.
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PMID:Changes of vasoactive substances following embolization for renal cell carcinoma. 322 30

The purpose of this study is to examine the relationship between lipid alterations in renal membrane of SHRSP and the progress of hypertension. Phospholipase A2 activity, prostaglandin E2 synthesis, phospholipids and phospholipid fatty acids were investigated in renal cortex and medulla of male SHRSP at the ages of 5, 10, 20 and 40 weeks, and compared with age-matched Wistar-Kyoto rats (WKY). In renal membrane of SHRSP, phospholipase A2 activity enhanced and PGE2 synthesis increased both in the renal cortex and the medulla after 20 weeks of age. Phospholipids, especially phosphatidylcholine and phosphatidylethanolamine, and arachidonate were decreased in cortex after 20 weeks and in medulla after 10 weeks. Moreover, to determine the effect of pressure load on lipid alterations, SHRSP that received an antihypertensive treatment with hydralazine or nicardipine or enalapril for 5 weeks were compared with those without treatment. Antihypertensive treatment prevented the blood pressure from rising and suppressed decreases of phospholipids and arachidonate in phospholipid. In conclusion, these results might suggest that enhanced phospholipase A2 cause by hypertension activate the arachidonic acid cascade and increase prostaglandin synthesis, which might have an homeostatic action to lower the blood pressure in SHRSP. On the other hand, decreases of phospholipids and arachidonate may provide an explanation for the membraneous structural abnormalities in SHRSP. Antihypertensive treatments prevent these alterations, though they have different actions in SHRSP.
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PMID:[Lipid alterations in renal membrane of stroke-prone spontaneously hypertensive rats (SHRSP)]. 324 Sep 23

We report that the inhibition of the angiotensin converting enzyme is an effective short-term treatment of low-renin hypertension in acute glomerulonephritis (AGN). We treated 9 patients who had AGN with moderate to severe hypertension and suppressed plasma renin activity with 25-50 mg of captopril per os every 6-8 hours. Control of blood pressure was achieved in 1-2 hours and maintained thereafter. Captopril therapy was associated with an increase in plasma renin activity, a decrease in plasma aldosterone and an increase in the urinary excretion of prostaglandin E2 and kallikrein, independent of changes in urine output. Creatinine clearance increased 39.6 +/- SE 15.2% with captopril and decreased in the postcaptopril period, suggesting that captopril exerted a reversible effect on glomerular filtration rate, possibly modifying intrarenal vasoconstriction. Our study shows that rapid control of hypertension in AGN may be obtained with oral inhibition of the angiotension converting enzyme. Stimulation of PGE2 and kinins, as well as angiotensin II blockade appear to contribute to the hypotensive effect of the drug; by inference, the suppressed activity of vasodilator systems seems to play a significant role in the hypertension of AGN.
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PMID:Short-term treatment with captopril in hypertension due to acute glomerulonephritis. 328 29

The renomedullary interstitial cell (RIC) is a unique cell found in the renal medullary interstitium among the collecting ducts, Henle's loop, and the vasa recta. A combination of morphologic and physiologic studies has defined some of the properties of this cell, which is the apparent source of the mediators of the antihypertensive function of the kidney. These may include prostaglandins (PGE2), APRL or platelet activating factor, and the incompletely defined neutral lipid, ANRL (or medullipin), the most likely candidate for this function. The lipid droplets in the RIC apparently are the precursors of the mediator(s). Degranulation of the RIC by an experimental maneuver usually indicates increased activity of these cells. The presence of abundant well-granulated RIC in a kidney indicates a resistance of that animal to the induction of salt-sensitive forms of experimental hypertension. There is definite evidence for an extrarenal antihypertensive function of the RIC mediators, but an intrarenal effect also is considered.
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PMID:Morphometric studies of the renomedullary interstitial cells. 328 48

The renal and systemic metabolites (the latter as 2,3-dinor derivatives) of prostacyclin and thromboxane A2 were measured, along with renal prostaglandin E2 and kallikrein, in the urine of 15 patients with pregnancy-induced hypertension, 15 normotensive pregnant women matched for both age and gestational age, and 15 normotensive nonpregnant control women. Urinary excretion of all prostaglandin and thromboxane metabolites studied proved significantly higher in normotensive pregnant women than in controls. Prostaglandin E2, 6-keto-prostaglandin F1 alpha, and 2,3-dinor-6-keto-prostaglandin F1 alpha were significantly lower in pregnancy-induced hypertensive women than in normotensive pregnant women, whereas thromboxane B2 and 2,3-dinor-thromboxane B2 showed no significant differences in the two groups. A significant negative correlation (r = -0.636, p less than 0.01) was found between urinary 2,3-dinor-6-keto-prostaglandin F1 alpha and mean blood pressure in the two groups of pregnant women taken as a whole. These data indicate that, in pregnancy-induced hypertension, there is an imbalance between vasodilator and vasoconstrictor factors, not only in the kidneys, but also at the systemic vascular level. This imbalance, which may in itself produce vasoconstriction, may also potentiate the hypertensive effect of catecholamines and angiotensin II.
Hypertension 1988 Jun
PMID:Altered excretion of prostaglandin and thromboxane metabolites in pregnancy-induced hypertension. 329 Jan 3

Phospholipase A2 activity and prostaglandin synthesis were studied in the renal cortex and medulla of stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched normotensive Wistar-Kyoto rats (WKY) aged 10-50 weeks. Enhanced phospholipase A2 activity was found in both the cortical and the medullary microsomes of SHRSP kidneys. Phospholipase A2 activity progressively increased with age in SHRSP, but not in WKY. Prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) were the major prostaglandins found in the cortex, and PGE2 was the major prostaglandin found in the medulla. Prostaglandin l2 (PGI2) was synthesized in both the cortex and medulla, but cortical PGI2 synthesis was much lower than medullary synthesis. Enzymatic activity for all prostaglandin syntheses analysed here were higher in SHRSP. There was a greater age-related increase in prostaglandin synthesis in SHRSP kidneys than in WKY kidneys. In addition, the ratios of PGE2/TXB2 and 6-keto-prostaglandin F1 alpha (PGF1 alpha)/thromboxane B2 (TXB2) decreased in SHRSP. This may produce vasoconstriction and increase vascular resistance in SHRSP. These data suggest that increased prostaglandin synthesis and phospholipase A2 activity have an important role in the development and maintenance of hypertension in SHRSP.
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PMID:Renal prostaglandins and phospholipase A2 in spontaneously hypertensive rats. 330 39

1. This study investigated the effects of dietary modification of prostaglandin (PG) synthesis on blood pressure regulation in DOCA/salt-treated rats. 2. After an initial 4 week period on either a 2-series PG 'inhibitory' diet of fish oil (Max EPA), A 'stimulatory' diet of safflower oil or a control diet of saturated fat, three groups of rats were placed on a DOCA/salt regimen for a further 4 weeks. Another group on the saturated fat diet continued their diet without DOCA/salt administration. 3. All the DOCA-treated groups showed a marked increase in blood pressure. However, both polyunsaturated fat (PUFA)-fed groups had blood pressures significantly lower then the saturated fat control. 4. Rats on the Max EPA showed impaired ability to generate prostanoids in vitro (serum, aorta and kidney) and in vivo (urinary PG excretion). DOCA administration increased urinary PGE2 excretion. 5. Thus, dietary suppression of 2-series PG is not accompanied by accelerated DOCA/salt hypertension. The reduction in blood pressure observed in both the safflower and Max EPA-fed groups may be due to PUFA-induced changes in cell membrane fluidity.
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PMID:Dietary suppression of prostaglandin synthesis does not accelerate DOCA/salt hypertension in rats. 331 35

A total of 154 patients with essential hypertension (EH), 24 patients with renovascular hypertension (RVH), and 130 Wistar rats were investigated. PGE2 and PGF2 alpha levels were assayed radioimmunologically in renal venous blood and urine of the patients, and the synthesis of PGE2 and PGF2 alpha in renal tissue, renal PGE-9-ketoreductase activity and urinary PG excretion were measured in rats. It was demonstrated that the PGE2 synthesis was depressed in the vascular channel and the renal uropoietic system, with elevated F/E rations, in patients with arterial hypertension. Clinical and experimental studies showed prolonged and excessive salt consumption to be a cause of these changes, rooted in suppressed renal biosynthesis of both PGs and increased conversion of PGE2 to PGF2 alpha. In addition, renal PGE2 inactivation was increased in EH patients, as compared to those with RVH. PGE2 produced in the kidneys of EH patients is always a depressor natriuretic substance, whereas the role of PGF2 alpha is dependent on the water-salt balance. Furosemide and, to a smaller extent, other diuretics, as well as some hypotensive agents, increase urinary PG excretion and depress the F/E ratio in the urine. Repeated PGE2 infusions are shown to enhance the sensitivity of EH patients to hypotensive drugs, so they can be used for the treatment of refractory EH cases.
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PMID:[Renal prostaglandins and hypertension]. 345 67


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