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

Plasma renin activity and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and four prostaglandins (PGE2, PGF2 alpha, 6 keto PFG1 alpha and TXB2) in 23 patients with pregnancy induced hypertension (17 with permanent PIH and six with labile PIH, since in these latter their hypertension was controlled only by home bed rest) and in 16 normotensive pregnant women at the same stage of gestation (31 +/- 3 weeks). PRA was lower in permanent PIH than in controls and in labile PIH. No difference between the three groups was observed for plasma aldosterone and the urinary excretion of kallikrein and of the prostaglandins except that TXB2 was higher in labile PIH than in permanent PIH. Correlation studies of kallikrein disclosed correlations with most prostaglandin excretions, explained by the physiological stimulation of phospholipase A2 by kallidin. Correlation studies of PRA disclosed unexpected negative correlation with PGE2 and 6 keto PGF1 alpha in the permanent PIH group. In conclusion, labile PIH has a different biological profile than permanent PIH since they have higher PRA and higher TXB2 excretion, an association which suggests a more pronounced ureteral compression by the gravid uterus in this group. Permanent PIH has a disregulation of the renin angiotensin-prostacyclin loop since PRA and 6 keto PGF1 are negatively correlated. This suggests the role of an independent vasopressive substance which would stimulate PGI2 and suppress renin secretion.
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PMID:Renin angiotensin aldosterone system, urinary prostaglandins and kallikrein in pregnancy induced hypertension. Evidence for a disregulation of the renin-angiotensin-prostacyclin loop. 384 87

Fifty-four hypertensive patients with the average BP level of 208 +/- 3.2/125 +/- 2.4 mm Hg were infused 2 doses of PGE. Forty patients received PGE2 in the form of protein (USA) and 14 patients were administered PGE1 in the form of alprostadil (USA). Each patient received on the average 3.5 mg of PGE2 or 0.7 mg of PGE1 during 48 hours. PGE infusion by the devised scheme induced no significant side-effects, was attended by an increase in the diuresis and natriuresis as well as a BP decrease (more pronounced with PGE1) not only in the period of the infusion but also during the 2-3 days following it. The hypotensive effect and BP fall in the orthostatic position were more marked following PGE2 infusion. PGE enhanced the sensitivity of the patients to obsidan, clophelin, hydrochlorothiazide and to a lesser degree to corinfar. Infusion of PGE2 to patients with essential hypertension resistant to hypotensive agents reduced the BP and made it possible to diminish the number of the drugs prescribed and their doses. The hypotensive effect of the drugs administered persisted for up to 5-7 months. It can be expected that repeated infusions of PGE2 every 6 months, will contribute to an alleviation of arterial hypertension, the patient's clinical improvement and the lowering of doses of hypotensive drugs.
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PMID:[Use of series E prostaglandins in the treatment of essential hypertension]. 385 1

This study examined the effect of diet-induced changes in prostaglandin synthesis on systolic blood pressure in one-kidney, one clip (1k, 1C) hypertensive rats and on the fall in blood pressure after unclipping. It tested the hypothesis that inhibition of prostaglandin synthesis exacerbates hypertension in this model and prevents complete reversal after unclipping. Rats with sustained hypertension within 8 weeks of renal artery clipping were fed synthetic diets supplemented to 20% of total energy with either safflower oil (linoleic acid) or a mixture of cod liver oil (90%) (containing eicosapentaenoic acid) and linseed oil (10%) (containing linolenic acid) for 4 weeks. The latter oil mixture resulted in a predictable reduction in kidney PGE2 and 6-keto PGF1 alpha (hydrolysis product of PGI2), aortic 6-keto PGF1 alpha and serum TXB2. However, at the end of 4 weeks dietary treatment there were no differences in systolic blood pressure between the two diet groups, and the blood pressure fall 24 hours after unclipping was similar. These findings therefore do not support a role for prostanoids in the maintenance or reversal of 1K, 1C hypertension.
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PMID:The effect of dietary alteration of prostaglandin synthesis on blood pressure and the reversal of hypertension in the one-kidney, one-clip rat. 385 91

The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1 alpha (stable degradation product of PGI2) was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 +/- 4 to 182 +/- 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1 alpha (from 31 +/- 4 to 43 +/- 5 ng/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 +/- 4 mmHg) and sham-denervated (211 +/- 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 +/- 3 and 147 +/- 4 mmHg, respectively). Urinary 6-keto-PGF1 alpha increased from 25 +/- 5 to 74 +/- 11 in denervated and 21 +/- 2 to 72 +/- 9 ng/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K,1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms.
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PMID:Renal prostanoids after unclipping the denervated one-kidney, one-clip hypertensive rat. 386 93

The purpose of the study was to clarify the mechanism(s) of glucocorticoid-induced hypertension. Hypertension was induced in rats by single i.m. injection of methylprednisolone (MP) 20 mg/kg. In normal Wistar rats, systolic blood pressure (SBP) increased by 30 mmHg from days 2 to 10 after MP. Urinary sodium excretion increased transiently and sodium balance was negative. Plasma volume (PV; ml/100 g body weight) increased on day 5, but was unchanged on day 2 after MP, at a time when SBP had already increased. In rats with chronic renal failure (CRF) and low sodium intake, SBP increased more than in control rats (48 versus 22 mmHg on day 10). Hypertension was not accompanied by a significant drop in urinary excretion of prostaglandin E2 (PGE2; measured by radio-immunoassay). In normal MP-injected rats, PGE2 excretion decreased slightly and then increased; in CRF rats, basal PGE2 excretion was too low to evaluate the effect of MP. In homozygous Brattleboro rats lacking antidiuretic hormone (ADH), MP increased SBP by 28 mmHg (day 10). Similar changes were obtained in heterozygous Brattleboro rats. The changes in PV were identical to those found in Wistar rats. We conclude that increase in PV, change in PGE2 and vasopressin do not play a key role in MP hypertension. Direct effect of glucocorticoid on vascular receptors is likely to be involved in this model.
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PMID:Methylprednisolone-induced hypertension in the rat: evidence against the role of plasma volume changes, vasopressin and renal prostaglandin E2. 386 57

Vascular reactivity was investigated in isolated perfused mesenteric vessels of young and adult SHR and age matched WKY. The primary objective was to investigate whether the difference in vascular reactivity between SHR and WKY would persist if endogenous prostaglandin synthesis was abolished and vascular reactivity restored with fixed exogenous quantities of PGE2. In young rats, when similar concentrations of PGE2 are infused in indomethacin blocked preparations, the difference in vascular reactivity between SHR and WKY is abolished. However, in adult rats the difference persists. It is concluded that enhanced prostaglandin synthesis in hypertension may participate in enhancing vascular reactivity.
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PMID:The effects of indomethacin and PGE2 on vascular reactivity in spontaneously hypertensive rats: possible role of prostaglandins in the pathogenesis of hypertension. 386 67

To clarify the metabolism of PGE2, prostacyclin (PGI2) and thromboxane A2 (TxA2) in small vessels in spontaneously hypertensive rats (SHR), we removed superior mesenteric vascular beds from 10 week old SHR and age matched normotensive controls (WKY). The mesenteric artery was perfused with Krebs-Henseleit buffer and samples of effluent collected every 15 minutes during 3 hours perfusion for analysis of PGE2, 6-keto-PGF1 alpha (a stable metabolite of PGI2) and TxB2 (a stable metabolite of TxA2) by specific radioimmunoassays. Levels of all three arachidonic acid (AA) metabolites, PGE2, 6-keto-PGF1 alpha and TxB2, in the mesenteric effluent were significantly reduced in SHR as compared to WKY. TxB2 was detected in all samples throughout the perfusion. 6-keto-PGF1 alpha/PGE2 ratios and TxB2/PGE2 ratios were significantly increased in SHR. 6-keto-PGF1 alpha/TxB2 ratios in the first four samples were significantly decreased in SHR as compared to WKY. These data suggest that there may be reduced availability of PG precusor AA and unbalanced synthesis of PGs in small vessels in SHR. Both may have relevance to the development of hypertension in the animals.
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PMID:Prostaglandins and thromboxane outflow from the perfused mesenteric vascular bed in spontaneously hypertensive rats. 388 20

To investigate the role of intrarenal prostaglandins in the pathophysiology of renovascular hypertension, we measured bilateral renal vein prostaglandins (PGE2, 6-keto-PGF1 alpha) and plasma renin activity (PRA) of nine patients with renovascular hypertension caused by fibromuscular dysplasia. Both PGE2 and PRA on the stenotic side were significantly higher than those on the non-stenotic side. The difference in 6-keto-PGF1 alpha levels between the stenotic and the non-stenotic sides was not significant. PGE2 ratio of the stenotic and the non-stenotic sides was significantly correlated with PRA ratio of the stenotic and contralateral sides. These results suggest that renal PGE2 plays an important role in the maintenance of renal blood flow through modulation against vasoconstriction in the renal vasculature and that renal PGE2 may be closely associated with renal renin secretion in the renovascular hypertension.
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PMID:Renal vein prostaglandins in renovascular hypertensive patients. 390 75

Increased sympathetic activity or vascular reactivity to norepinephrine or both may play a complementary role in the pathogenesis of essential hypertension. Therefore, blood pressure regulation and metabolic correlates of cardiovascular risk were evaluated in 19 normal subjects and in 13 subjects with essential hypertension receiving placebo and after 4 weeks of intervention with urapidil, an agent that was found experimentally to exert a combined central sympathetic and peripheral alpha-adrenergic receptor inhibition. In hypertensive patients, urapidil normalized the initially low norepinephrine pressor dose (+ 106%), mildly increased basal plasma norepinephrine levels (+36%), and markedly shifted the plasma norepinephrine concentration-blood pressure response curve (p less than 0.01). Blood pressure was decreased (p less than 0.001). In normal subjects, urapidil produced only mild increases in norepinephrine plasma levels (+22%) and norepinephrine pressor dose (+38%) and no change in blood pressure. Body weight, exchangeable sodium, and blood volume were unaltered or increased slightly. Heart rate; plasma epinephrine, renin, angiotensin II, basal aldosterone, and electrolyte levels; plasma clearances of norepinephrine and angiotensin II; pressor effects of angiotensin II; chronotropic responses to isoproterenol or a norepinephrine-induced rise in blood pressure; and urinary prostaglandin F2 alpha excretion, as well as serum lipoprotein fractions and glucose, insulin, and uric acid levels, were not significantly modified by urapidil. Prostaglandin E2 excretion tended to be increased. Aldosterone responsiveness to angiotensin II was increased by urapidil in normal (p less than 0.05) but not in hypertensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Cardiovascular and metabolic profile during intervention with urapidil in humans. 390 16

As platelet and renal thromboxane (TX)A2 synthesis are increased in spontaneously hypertensive rats (SHR), we tested the hypothesis that increased renal TXA2 synthesis may cause the reduction in glomerular filtration rate (GFR), renal plasma flow (RPF), and the increase in arterial pressure in SHR of the Okamoto-Aoki strain. A selective inhibitor of TXA2 synthetase (UK 38485) was given acutely, with or without a TXA2 receptor antagonist (EP-092), to 6- to 8-wk-old SHR and age-matched Wistar-Kyoto rats (WKY) and chronically for 5.5 wk to 3.5-wk-old SHR. Inhibition of TXA2, measured by the stable metabolite TXB2, in the acute experiments was greater than 95% in serum and greater than 80% in glomeruli; in the chronic studies, it was greater than 65% in glomeruli. There was no endoperoxide shunting to vasodilatory and natriuretic prostaglandins (PGE2, PGI2) in glomeruli after TXA2 inhibition. Before drug administration, GFR and RPF were reduced and renal vascular resistance (RVR) was increased in SHR. During acute blockade of renal TXA2 synthesis, with or without a TXA2 receptor antagonist, there was no significant change in GFR, RPF, or RVR in WKY and SHR. Inhibition of TXA2 did not affect urine flow or sodium excretion in anesthetized or conscious WKY or SHR. Mean arterial pressure did not fall in treated SHR and WKY. Chronic TXA2 synthesis inhibition did not improve GFR or RPF in SHR, and systolic arterial pressure was not altered. These findings show that enhanced serum and glomerular TXA2 synthesis do not significantly contribute to the reduction in renal function and are not essential for the development of hypertension in young SHR.
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PMID:Role of thromboxane in control of arterial pressure and renal function in young spontaneously hypertensive rats. 395 27


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