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

PG A1, B1, E2, F1,2alpha and PRA have been measured in 8 hypertensive patients with unilateral renal arterial stenosis, 7 hypertensive patients with unilateral renal atrophy and 20 control normotensive subjects. PRA and PGA1 were significantly increased in patients with renovascular hypertension but not in patients with atrophy. PGE2 and PGF1,2alpha were increased in both groups of patients, especially on the stenotic or atrophic side. The increase of PGA1 and PGE2, represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF1,2alpha a direct hypertensive mechanism.
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PMID:Prostaglandins in renovascular and renal hypertension. 69 90

1. Hypertension produced in two-kidney Goldblatt dogs was accompanied by a transient fluid retention, reaching a maximum 4 days after clamping. 2. Prostaglandin E and F concentrations in venous blood from the intact kidney also rose transiently, showing a maximum by the fifth day. 3. The rise in prostaglandin release from the intact kidney may be related to the fluid retention.
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PMID:Renal prostaglandins in renal hypertensive dogs. 75 Jan 58

1. Renal prostaglandins act primarily as local hormones, having their effects at, or near to, sites of synthesis. PGE2 is a major determinant of renal vascular reactivity; it opposes the vasoconstrictor and natriuretic actions of pressor hormones and brakes the release of noradrenaline from adrenergic nerves. In the unanaesthetized rabbit prolonged inhibition of prostaglandin synthesis results in hypertension. In the rat, however, renal prostaglandins augment pressor stimuli. 2. Basal efflux of renal prostaglandins is positively correlated with blood flow to the inner cortex and medulla. Those stimuli which increase renal medullary blood flow do so primarily by activating prostaglandin synthetase. 3. Kinins increase prostaglandin synthesis which action modifies the renal effects of kinins. Thus, one or more renal prostaglandins contribute to the renal vasodilator action of bradykinin and mediate its effect on excretion of water as well as possibly attenuating the natriuretic action of the polypeptide. Kinins in addition to stimulating prostaglandin synthesis may determine the principal product of synthetase by regulating the enzyme PGE 9-ketoreductase, which converts PGE to PGF. The coupling of these systems within the kidney appears unique--prostaglandins mediate some of the actions of kinins and modulate others, whereas they depend on the intrarenal generation of kinins to set their level and type of activity.
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PMID:Renal prostaglandins. 82 36

Fetal hypoxia secondary to uterine vascular insufficiency was induced by injecting norepinephrine or PGE2 into the maternal circulation of near-term sheep. With these drugs the uterine blood flow fell to 41 and 40% of its control value, respectively. The fetal responses to the PGE2-induced uterine contraction were a bradycardia which was apparent within 10 seconds (P less than 0.05), and a hypertension which was also apparent within 10 seconds (P less than 0.03). After the norepinephrine-induced uterine vasoconstriction, there was no observable change in the fetal arterial pressure. The fetal heart rate started to fall after 30 to 60 seconds and started to return to the control value within 90 seconds. The fetal response to uterine vascular insufficiency induced by a contraction may not have been caused by hypoxia alone as these responses were more rapid in onset than the fetal responses observed subsequent to uterine vascular insufficiency produced by vasoconstriction.
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PMID:The effect of uterine vascular insufficiency on fetal arterial pressure and heart rate in the near-term sheep. 89 99

The realtionship between in vitro prostaglandin production by renal medullary tissue and hypertension was investigated in three models of hypertensive rat, i.e., DOCA, Goldblatt and SHR. Medullary minces were incubated for 30 minutes. Following incubation tissue PGE2 concentration was quantified using mass fragmentography. Media PGE2 concentrations were quantified using radioimmunoassay. Concentrations of PGE2 in tissue from Goldblatts and SHRs were significantly less than normotensive controls. The concentration of PGE2 in media after incubating SHR tissue was significantly less than normotensives. The data suggest that alterations in PGE2 metabolism are similar in Goldblatt and SHR hypertension.
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PMID:Prostaglandin E2 production by renomedullary tissue of DOCA, Goldblatt and spontaneously hypertensive rats. 100 18

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
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PMID:Renal prostaglandins. 110 Oct 92

Keeping in mind the vasodilator action of prostaglandins, the control that they exercise over the vascular supply of kidneys and the sympathetic activity, research was conducted in order to establish the effect of arachidonic acid, the precursor of PGE2, on experimental hypertension in the rat. The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. The treatment was short in one group, long in the other, and both groups were compared to a control hypertensive group which received no treatment at all. Arachidonic acid worsened the experimental hypertension by 37% in the long treatment, and by 25% in the short treatment. The administration of lysine-acetylsalicylate diminished this hypertension. A non-saturated acid, oleic acid, which is not involved in prostaglandin synthesis, has no action. The authors would like to emphasize that in one of the previous experiments, L-tyrosine, the precursor of catecholamines, diminished the experimental hypertension in the rat, and also that L-DOPA and IMAO (MAOI) have comparable effects. It seems, therefore, that the depression of the central catecholaminergic activity, which is supposed to be the action of arachidonic acid via an increase in the PGE2 synthesis, appears to increase hypertension. It is noteworthy that the medial forebrain bundle (MFB) is catecholaminergic and that the periventricular system (PVS) is cholinergic. Thus hypertension may represent the peripheral vascular response to anguish which results from the activation of PVS and from the depression of MFB.
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PMID:The action of arachidonic acid on experimental hypertension in the rat. 112 60

A parallel study of plasma renin activity, renin content in the kidneys and renal prostaglandin - like activity (PGE2, A2 and F2alpha) in 10 spontaneously hypertensive (SHR) rats (Pkamoto-Aoki), and 10 control normotensive Wistar rats was carried out in order to investigate the role of humoral factors in the pathogenesis of spontaneous hypertension in rats. Peripheral plasma renin activity was assayed by the method of Serebrovskaya, while renal renin activity was estimated by the author's own modification of the method of Serebrovskaya. Prostaglandin-like activity of the renal prostaglandins was assayed by the method of Lee et al. The final evaluation of the PGE2 and PGF2alpha activity was made by biological assay on isolated rat stomach and chicken rectum strips, while PGA2 - like activity was assayed by its vasodepressor effect on the arterial blood pressure of anaesthetized, vagotomized and atropinized rats. It was established that peripheral plasma renin activity was normal, while renin activity in the kidneys of SHR with a long (11 months) duration of hypertension was decreased. Renal prostaglandin activity of SHR did not significantly differ from the controls. It is pointed out that lack of changes in the pressor and depressor renal systems indicates that renal humoral factors are not of prime importance in the patho-genesis of the chronic stage of spontaneous hypertension in rats.
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PMID:Vasodepressor activity of renal medulla of spontaneously hypertensive rats. 115

Hypertension is the main side effect developing in patients suffering from renal anemia who are treated with recombinant human erythropoietin (rhEPO). We investigated the effect of rhEPO on the vascular tone of rabbit aorta. rhEPO had no direct vasoconstrictor effect, but it enhanced norepinephrine (NE)-induced contractions of rabbit aortic rings. Relaxations to acetylcholine (ACh, 1 microM) were unaltered in the presence or absence of rhEPO, indicating that the endothelium-dependent NO pathway was not affected by rhEPO. In rings of human renal artery and rabbit aorta, rhEPO (200 U/ml) increased the synthesis of constrictor prostanoids. The cyclooxygenase inhibitors indomethacin and aspirin abolished the increase in prostanoid production. However, they did not completely suppress the rhEPO-induced enhancement of NE contractions in rabbit aorta. We further investigated the effect of rhEPO on prostanoid and endothelin-1 synthesis in cultured human endothelial cells. Endothelial cells from human umbilical veins (HUVEC) were isolated and cultured. After incubation with rhEPO, the formation of prostaglandin (PG) I2 (analyzed as its stable metabolite 6-keto-PGF1 alpha), PGF2 alpha, PGE2, thromboxane (Tx) B2, and of endothelin-1 (ET-1) was measured by radioimmunoassay (RIA). rhEPO (200 U/ml) increased the formation of PGF2 alpha and TxB2 and decreased the formation of PGI2 in HUVEC. The release of ET-1 was increased by nearly 90% in the presence of rhEPO (200 U/ml). We conclude that a shift in the balance of constrictor and relaxing prostanoids as well as an increased synthesis of ET-1 may contribute to the hypertensive side effect of rhEPO therapy. ET-1 may at least in part be responsible for the unexpectedly low inhibitory effect of indomethacin on rhEPO-enhanced contractions of rabbit aorta.
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PMID:Endothelin release and shift in prostaglandin balance are involved in the modulation of vascular tone by recombinant erythropoietin. 128 78

After two weeks' treatment of indapamide (2.5 mg/d) in 30 cases of mild to moderate hypertensive patients, there was a significant decline of systolic and diastolic blood pressure. And 8 weeks after indapamide administration, 2/3 of the total treated patients achieved complete control of hypertension. During the treatment period, there were no changes of serum cholesterol, triglyceride and renal function, except a slight, but still in the normal range, decrease of serum potassium and sodium. Concurrently, plasma vasoconstrictive prostaglandins TXB2 (metabolite of TXA2) and PGF2 alpha reduced significantly (P < 0.01 and P < 0.001 respectively), whereas plasma vasodilative prostaglandins 6-keto-PGF1 alpha (metabolite of PGI2) and PGE2 increased significantly (P < 0.02 and P < 0.05 respectively). The results support the theory that prostaglandins system may play an important role in the hypotensive process of indapamide. The influence of indapamide on prostaglandin system may favour the improvement of platelet function and the maintenance of the homeostasis.
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PMID:[The effect of indapamide on plasma prostaglandins in hypertensive patients]. 130 70


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