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

Previous investigations have shown that brain prostaglandin levels are transiently elevated following experimental fluid percussion brain injury. Associated with these increased prostaglandin levels there is free radical production and abnormalities in cerebral arteriolar function. The purpose of this study was to determine whether experimental fluid percussion brain injury in cats is associated with increased systemic levels of prostaglandins and the lipoxygenase product, 12-HETE. Blood samples were collected before and at various periods of time after 2.7 atm of fluid percussion brain injury was produced in adult cats. Prostaglandin and 12-HETE analysis was performed by radioimmunoassay after extraction of the plasma samples. The control levels for 6-keto-PGF1 alpha, PGE2, and 12-HETE were 477 +/- 42, 2,372 +/- 431, and 13,328 +/- 1,769 pg/ml, respectively. Following injury all three eicosanoids reached peak plasma levels by 1-5 min after injury. The percentile increases for all eicosanoids were similar and increased from 70 to 110%. The increases were sustained at up to 30 min postinjury and by 1 h after injury were at control levels. As in previous studies, hypertension following injury was maximal by 1 min postinjury and blood pressure had returned to near normal levels by 5 min postinjury. These studies demonstrate prolonged systemic increases in eicosanoids following injury. Since free radical production and vascular damage occur concomitantly with eicosanoid production, the prolonged increases in these products suggest that there is an attainable therapeutic window following injury during which administration of free radical scavengers may decrease radical damage and reduce the consequences of injury.
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PMID:Increased plasma PGE2, 6-keto-PGF1 alpha, and 12-HETE levels following experimental concussive brain injury. 250 34

Cicletanine is a new antihypertensive agent known for being able to stimulate prostaglandin synthesis in vivo and in endothelial cell cultures. The drug was administered to spontaneously hypertensive rats (SHP-SP) whose hypertension was enhanced by a high sodium content diet. Cicletanine prolonged the animals' survival and reduced the severity of histological renal lesions. PGE2, PGI2 and thromboxane A2 assays performed in renal tissues showed a highly significant increase of PGE2 (a prostaglandin involved in the regulation of renin synthesis) in SHR-SP rats treated with oral cicletanine in daily doses of 30 mg/kg. A less significant increase of PGI2 was found in renal tissues, whereas only slight variations in thromboxane concentrations were observed. The favourable therapeutic effect obtained with cicletanine in the treatment of hypertension may be due, at least in part, to the stimulation of PGE2 and PGI2 production in renal tissue.
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PMID:[Effects of treatment with cicletanine on kidney PGE2 and PGI1 in spontaneously hypertensive rats]. 251 66

The purpose of this study was to evaluate the level of renal synthesis of vasodilator and natriuretic prostaglandins I2 and E2 in patients with essential hypertension and to test the effect of cicletanine, a new antihypertensive drug, on the renal synthesis of these prostanoids in hypertensive patients. The first part of the study was carried out in 12 healthy normotensive subjects and in 25 patients of both sexes with essential hypertension. The effect of cicletanine administered in dose of 150 mg was assessed in 10 healthy volunteers and 12 hypertensive patients. The urinary levels of prostaglandins 6-keto-PGF1 alpha (a metabolite of prostacyclin PGI2) and PGE2 were measured (HPLC) by radioimmunoassay after extraction and chromatographic separation. In normal subjects the urinary excretion rate of 6-keto-PGF1 alpha was 134 +/- 26 pg/min and that of PGE2 was 180 +/- 25 pg/min. The corresponding values were significantly lower in hypertensive patients. This defect of PGI2 and PGE2 renal synthesis was found in 64 p. 100 and 72 p. 100 respectively of patients with hypertension. Cicletanine increased the urinary excretion of 6-keto-PGF1 alpha by 45 p. 100 and that of PGE2 by 59 p. 100 in hypertensive patients. It also brought to normal limits the secretion of these prostanoids in these subjects. At the dose of 150 mg the drug stimulated natriuresis significantly and increased glomerular filtration in patients with essential hypertension. This renal effect of cicletanine was acutely reduced by the presence of indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Reduction of kidney prostaglandin synthesis in patients with essential hypertension. Stimulating effect of cicletanine]. 251 74

Neonatal calves exposed to chronic hypobaric hypoxia develop severe pulmonary hypertension associated with altered vascular reactivity, cellular proliferation, and increased elastin and collagen production. We hypothesized that prostaglandin (PG) production would be decreased in the pulmonary arterial vessel wall of these calves. Further, because of the possibility that the hemodynamic stresses of hypoxic pulmonary hypertension might change along the longitudinal axis of the pulmonary circulation, we measured prostaglandin synthetic capability in tissues isolated from proximal pulmonary artery, distal pulmonary artery, and pulmonary vein. We found that PGI2 production was decreased in both proximal and distal pulmonary artery rings isolated from pulmonary hypertensive calves compared to controls. PGI2 production was greater in distal than in proximal lobar pulmonary artery. In contrast, pulmonary veins from hypertensive calves, which are protected from the hemodynamic stress of pulmonary arterial hypertension, did not demonstrate altered PGI2 production compared to controls. PGE2 production was also decreased in proximal hypertensive pulmonary arterial rings as compared to controls. To determine if this decrease in vessel wall production of prostaglandins was due to changes in cellular prostaglandin production, we studied prostaglandin production by the three major cell types comprising hypertensive and control arteries. Endothelial cells cultured from hypertensive main pulmonary artery produced less PGI2 than did those from control artery, and there appeared to be a shift from PGI2 production to PGE2 production in endothelial cells isolated from hypertensive artery. Explanted advential fibroblasts from hypertensive artery produced less PGE2 than did controls. Smooth muscle cell PGI2 production did not differ between cells isolated from hypertensive and control arteries in these brief 30-min incubations. We conclude that there is a relative deficit in PGI2 and PGE2 production in the pulmonary arteries of calves with hypoxia-induced pulmonary hypertension and speculate that this contributes to altered vascular tone and vessel remodeling.
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PMID:Decreased arterial wall prostaglandin production in neonatal calves with severe chronic pulmonary hypertension. 251 77

The effect of i.v. bolus administration of PGE2 and PGF2 alpha on carotid blood flow (Q) and mean arterial blood pressure (MAP) was recorded in 21 anaesthetized normotensive control (N) and 12 rats with 1K1C renovascular hypertension (RH). From the measured parameters the regional vascular impedance (PVI) and the change in blood volume were calculated. In normotensive animals both PGs elicited a dose-dependent initial fast increase of Q (threshold dose 0.4 ng/kg) and a decrease of MAP and PVI (threshold dose 0.4 micrograms/kg). Subsequently, Q decreased below the initial level. MAP and PVI remained depressed after E2 but increased after F2 alpha. The time course of the Q and MAP responses was analyzed in more detail at a standard dose 4 micrograms/kg. The average time to peak of the first phase was 12 s and of the second approximately 80 s. The initial levels of Q and MAP were reestablished within 3 to 4 minutes. The total volume of carotid blood flow obtained by planimetric integration was unaltered after F2 alpha but depressed after E2. In hypertensive animals both phases of the response to E2 were significantly retarded and the Q response was nearly abolished. On the other hand, the time course of the reaction to F2 alpha was unchanged but the magnitude of the second pressoric phase was reduced. Thus, the capacity of the carotid vascular bed to dilate remains the same in RH while the ability to constrict is limited. It is concluded that the response of MAP and Q to both PGs are relatively independent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of prostaglandins E2 and F2 alpha on carotid blood flow in rats with renovascular hypertension. 253 87

Polyunsaturated fatty acids of the omega-6 and the omega-3 series have been shown to lower arterial pressure in humans and in various models of experimental hypertension by uncharacterized mechanisms. The objectives of our study were to compare the antihypertensive properties of linoleic acid (omega-6 series) and of fish oil fatty acids (omega-3 series) in a model of hypertension induced by the continuous subcutaneous infusion of angiotensin II in the rat and to determine whether or not their antihypertensive effects were mediated by the biosynthesis of vasodilator prostaglandins of classes 2 or 3. Linoleic acid and fish oil fatty acids (administered by subcutaneous injections) were equally potent in reducing, by half, the rise in systolic arterial pressure induced by the chronic infusion of angiotensin II. These antihypertensive effects were observed in the absence of any significant influence of either linoleic acid or fish oil fatty acids on the systemic and the renal synthesis of PGI2 or on the renal formation of PGE2 in vivo. Indomethacin caused a profound inhibition of the biosynthesis of PGI2 but not of PGE2 and could only partially neutralize the antihypertensive effects of linoleic acid and of fish oil fatty acids. These results suggest that, in this model of angiotensin II-induced hypertension, linoleic acid and fish oil fatty acids exert equipotent antihypertensive effects which are mainly independent of the prostaglandin system.
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PMID:Antihypertensive properties of linoleic acid and fish oil omega-3 fatty acids independent of the prostaglandin system. 255 31

To elucidate mechanisms of angiotensin II (Ang II)-related hypertension, we infused angiotensin (76 ng/min s.c.) into rats with minipumps for 10-14 days. Control rats received sham pumps. We measured blood pressure by tail-cuff, and the excretion of aldosterone and prostaglandins (PG) (PGE2, prostacyclin derivative 6kPGF1 alpha, and thromboxane [Tx] derivative TxB2). Angiotensin II increased blood pressure by 20 mm Hg by day 2 and by 90 mm Hg by day 10. Aldosterone excretion increased from 10 to 70 ng/day in Ang II rats by day 7. Urine PGE2 did not increase in angiotensin rats; however, both 6kPGF1 alpha and TxB2 excretion increased with angiotensin. Control rats had no changes in any of these parameters. A sympathetic component was tested in a separate group of angiotensin rats that received phenoxybenzamine (300 micrograms/kg/day) during angiotensin infusion; their increase in blood pressure of 40 mm Hg at 10 days was less than in those rats with angiotensin alone but more than in control rats. Phenoxybenzamine did not influence the angiotensin-induced increases in excretion of 6kPGF1 alpha or TxB2. Additional groups of conscious angiotensin and control rats were equipped with splanchnic nerve electrodes on day 14 for recording of sympathetic nerve activity. Angiotensin rats had greater basal sympathetic nerve activity than the control rats. Incremental methoxamine injections demonstrated altered baroreceptor reflex function in rats receiving angiotensin. We conclude that increased blood pressure with chronic angiotensin infusion is accompanied by increased production of aldosterone and increased sympathetic tone. The latter may be modulated by PG.
Hypertension 1989 Oct
PMID:Angiotensin-induced hypertension in the rat. Sympathetic nerve activity and prostaglandins. 255 21

Inhibition of cyclooxygenase enhances mesenteric vascular responses to periarterial (sympathetic) nerve stimulation (PNS) in 16-week-old spontaneously hypertensive rats (SHR), but not in 25-week-old SHR. In contrast, cyclooxygenase inhibition enhances mesenteric vascular responses to PNS similarly in 16- and 25-week-old Wistar-Kyoto normotensive rats (WKY). Thus, the modulation of noradrenergic neurotransmission by endogenous PGs becomes defective as SHR age, whereas in WKY this does not occur. The purpose of this study was to determine to what extent alterations in the concentrations of PGs and/or biological response to PGs contribute to this age/hypertension-related abnormality in SHR. All studies were conducted in the in situ autoperfused rat mesentery, and plasma levels of PGE2 and 6-keto-PGF1 alpha were determined by negative-ion, chemical-ionization, gas chromatography-mass spectrometry after derivatization and clean-up of samples by two thin-layer chromatographic steps. Base-line mesenteric venous plasma levels of PGs were similar in 16-week-old SHR vs. 16-week-old WKY; however, base-line levels of PGE2 were approximately 6-fold greater than base-line levels of 6-keto-PGF1 alpha in both strains. PNS at 7 Hz approximately doubled mesenteric venous plasma levels of PGE2 in both 16-week-old SHR and WKY, but PNS did not increase levels of 6-keto-PGF1 alpha in either strain. Inasmuch as mesenteric venous plasma levels of PGE2 were responsive to PNS, the effect of aging on PGE2 levels was studied. In both strains, the base-line mesenteric venous plasma levels of PGE2 and the PNS-induced increase in PGE2 levels were similar in 16-week vs. 25-week-old animals. In 16-week-old SHR, infusions of PGE2, arachidonic acid and PGI2 directly into the mesenteric artery inhibited vascular responses to PNS. However, in 25-week-old SHR, even high doses of PGE2 or arachidonic acid failed to inhibit vascular responses to PNS, and the inhibitory potency of PGI2 was shifted 10-fold to the right compared to 16-week-old SHR. In contrast, PGE2 and arachidonic acid had similar effects on neurotransmission in 25-week-old WKY compared to 16-week-old WKY, and aging had a lesser effect on the inhibitory potency of PGI2 (i.e., 3-fold rightward shift of the dose-response curve). Adenosine also inhibited vascular responses to PNS; however, the inhibitory potency of adenosine was only slightly and similarly affected by aging in SHR and WKY.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Defective modulation of noradrenergic neurotransmission by exogenous prostaglandins in aging spontaneously hypertensive rats. 255 20

Reversal of one-kidney, one clip (1-K, 1C) hypertension by removal of the renal artery clip is accompanied by increased renal and vascular prostaglandin (PG) production. It was postulated that PG biosynthesis is stimulated in the unclipped hypertensive kidney. In order to test this hypothesis, we compared urinary excretion of PGE2 and 6-keto-PGF1 alpha (a breakdown product of PGI2) in perfused kidneys isolated from 1-K, 1C hypertensive rats, 1-K, sham-clipped rats and 1-K, 1C rats which had failed to become hypertensive. Urine was collected over 15 min periods at perfusion pressures of 100, 150 and 200 mmHg. At perfusion pressures of 100 and 150 mmHg there was no significant difference in PGE2 excretion between the three groups. In contrast, 6-keto-PGF1 alpha excretion at 150 mmHg was higher in the hypertensive rats compared with the sham-clipped (P less than 0.05) and failed hypertensive (P less than 0.01) rats. At 200 mmHg, both PGE2 and 6-keto-PGF1 alpha were significantly higher in the hypertensive rats than in the control groups. These increases in PG excretion were clearly dissociated from changes in urinary flow rates. The findings support the hypothesis of increased synthesis of renal vasodilatory and natriuretic PGs in 1-K, 1C hypertension which is particularly evident at higher perfusion pressures, such as may be encountered when the hypertensive kidney is unclipped and exposed to high arterial pressure.
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PMID:Increased prostaglandin synthesis in the unclipped kidney of one-kidney, one clip hypertensive rats. 260 43

The effects of dietary K (food and tap water both containing 1% KCl) on blood pressure and renal prostaglandin-kallikrein-kinin system were investigated in Wistar rats made hypertensive by constriction of left renal artery. Dietary K attenuated the development of hypertension and increased urine volume accompanied by increased excretion of K, but by uninfluenced excretion of Na. Dietary K also increased the urinary excretion of kallikrein, PGE2 and aldosterone in Goldblatt hypertensive rats. There was no significant difference in the values of plasma Na between the two groups with and without dietary K. These results suggest that dietary K may attenuate the development of hypertension, increase urine volume via the mechanism of enhancing production of renal PGE2 and kallikrein in hypertensive rats.
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PMID:[Effects of dietary K on blood pressure, prostaglandin, and kallikrein in renovascular hypertensive rats]. 261 29


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