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

Prostaglandin (PG) I2 and PGE2 are known to stimulate left ventricular receptors with nonmyelinated vagal afferents. The present experiments were performed to determine the effects of intracoronary infusion of PGE2 (10-50 ng.kg-1.min-1) and arachidonic acid (50-100 micrograms.kg-1.min-1) on the baroreflex control of heart rate in conscious dogs. Dogs were anesthetized with pentobarbital sodium and were instrumented using sterile surgical techniques. After recovery, baroreflex pressure-heart rate curves were constructed by varying arterial pressure with partial occlusions of the descending aorta or inferior vena cava. Intracoronary infusion of PGE2 significantly inhibited the maximum heart rate achieved during unloading of baroreceptors, attenuated the heart rate range, and decreased the maximum slope of the baroreflex curve; PGE2 had no significant effect on the minimum heart rate during hypertension. Intravenous infusion of PGE2 did not cause significant baroreflex inhibition, and pericoronary nerve block in three dogs prevented the effects of intracoronary PGE2. Intracoronary infusion of arachidonic acid had effects on the baroreflex control of heart rate similar to those of PGE2. The effects of arachidonic acid infusion were prevented by cyclooxygenase blockade. Thus intracoronary PGE2 and arachidonic acid inhibit the baroreflex control of heart rate most likely via stimulation of left ventricular receptors with vagal C-fiber afferents. The effects of arachidonic acid were secondary to synthesis of prostaglandins.
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PMID:PGE2 and arachidonate inhibit the baroreflex in conscious dogs via cardiac receptors. 249 39

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

Urinary TXB2 excretion and the release of TXB2 from vascular and renal cortical tissues are increased in rats with severe AII-salt hypertension. Treatment with an inhibitor of TXA2 synthesis did not change the blood pressure of normotensive or of AII-salt hypertensive rats. Treatment with SQ29,548, a TXA2 receptor antagonist, caused reduction of blood pressure and renal vascular resistance in AII-salt hypertensive but not in normotensive rats. We conclude that the SQ29,548-induced lowering of blood pressure and renal vascular resistance in AII-salt hypertensive rats is the result of blockade of the vascular actions of one or more pressor eicosanoids including TXA2 and the prostaglandin endoperoxides. A corollary of this conclusion is that pressor eicosanoids may be contributory factors in the pathogenesis of severe AII-salt hypertension in rats.
Adv Prostaglandin Thromboxane Leukot Res 1989
PMID:Role of TXA2 in the pathogenesis of severe angiotensin II-salt hypertension. 252 69

A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
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PMID:The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome). A pathophysiological study. 297 68

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

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.
Hypertension 1987 Nov
PMID:Role of prostaglandins and kinins in the renal pressor reflex. 366 64

Prostaglandin-dependent, frusemide-induced changes in renal plasma flow, glomerular filtration rate and plasma renin activity were measured in 14 patients with mild essential hypertension. The renal haemodynamic responses to frusemide were the same as in 10 normal subjects. Frusemide-induced changes in urinary PGE and kallikrein excretion were also the same as in normal subjects. Impaired renal release of vasodilator prostaglandins in essential hypertension is likely to be secondary to the hypertension rather than an underlying factor in its development.
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PMID:Haemodynamic and endocrine responses of the kidney to frusemide in mild essential hypertension. 388 Dec 8

Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The animals were treated with dexamethasone or its vehicle (sesame oil) for 1 day (1.8 mg/kg) and for 14 days (1.8 mg/kg/wk). The superior mesenteric artery with its branches was isolated and perfused with Tyrode's solution at a constant flow rate of 5 ml/min. Administration of norepinephrine (1-10 nmol), arginine vasopressin (0.03-0.3 nmol), or angiotensin II (0.1-1 nmol) produced vasoconstriction and increased the output of 6-keto-prostaglandin F1 alpha and prostaglandin E2 in a dose-related manner in mesenteric vessels. Administration of 10 nmol bradykinin or 19 nmol A23187 enhanced the output of prostaglandins without altering vascular tone. The vasoconstrictor response to arginine vasopressin, but not norepinephrine or angiotensin II, was enhanced in mesenteric vessels from rats treated with dexamethasone for 14 days but not for 1 day. In contrast, the output of basal as well as norepinephrine, arginine vasopressin, angiotensin II, bradykinin, or A23187-induced prostaglandin output was significantly reduced in mesenteric vessels from rats treated with dexamethasone for 1 or 14 days. Prostaglandin output in mesenteric arteries from rats treated with dexamethasone for 1 and 14 days was not different. These data indicate that dexamethasone treatment for longer but not for shorter periods results in a selective increase in vascular reactivity of mesenteric vessels to arginine vasopressin that is independent of prostaglandin synthesis. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension.
Hypertension
PMID:Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats. 403 47

Prostaglandin research has been 1 of the most stimulating features of biomedical investigation in the past decade. Interest developed at a time of expanding knowledge of hormonal and neurohormonal behavior and research work received a tremendous impetus in the early 1960s with the elucidation in Sweden of the chemical structures of prostaglandins, followed by the discovery of their biosynthetic pathways. The original findings of large amounts of prostaglandin in the male accessory genital glands and their secretions, and subsequent discovery in the menstrual and amniotic fluids linked these substances with human production. As a result of further investigation, clinical applications of prostaglandins for the induction of labor and termination of early unwanted pregnancies have been developed. Apart from the functions of the prostaglandins in the reproductive area, they have been shown to have a widespread distribution in the body and produce many different pharmacological effects. Prostaglandins are thought to be involved in the regulation of blood pressure and through their vascular effects have therapeutic potential in the treatment of hypertension and peripheral vascular disease. Through their bronchodilator effect, some prostaglandins may become useful in the treatment of asthma.
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PMID:Prostaglandins: pharmacology and clinical application. 461 42

Our experience with the subclavian flap repair for coarctation of the aorta over the past 10 years includes 53 patients under 1 year of age. Of this group, 35 were newborn infants. All but two had an associated patent ductus arteriosus and 23 (66%) had associated intracardiac anomalies. All neonates had severe congestive heart failure and operation was carried out promptly after they were stabilized with diuretics and inotropic agents. Prostaglandin infusions have been essential to the care of many of these patients. Operative mortality was two of 53 patients (4%). No patient more than 4 days old operation has died, and concomitant pulmonary artery banding was performed in five infants with no deaths. Running nonabsorbable suture was used in 21 patients, interrupted nonabsorbable suture in 23, and continuous monofilament absorbable suture in the last nine. Mean follow-up time has been 46 months. Invasive follow-up studies, performed in 11 patients, have revealed residual systolic gradients of 5, 15, and 20 mm Hg in three and 0 mm Hg in one in whom continuous suture technique was used. The other seven had interrupted suture technique, and no gradient was present. Initial follow-up information for the group with absorbable suture repair suggests no residual gradients. No patient had significant upper extremity or hand morbidity. Eight patients had normal blood pressure and normal arm-to-leg gradients after exercise. When absorbable vascular suture is unavailable, an interrupted suture technique is superior to a continuous running repair. In view of the low operative mortality, the excellent growth of the repaired area, yet the likelihood of late development of cardiovascular disease (especially hypertension) if the repair is effected in childhood or adolescence, we favor prompt subclavian flap repair of coarctation of the aorta in all infants with or without symptoms. Concomitant pulmonary artery banding is seldom indicated.
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PMID:Should elective repair of coarctation of the aorta be done in infancy? 650 21


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