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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma renin reactivity (PRR) is the rate of angiotensin generation in vitro after addition of exogenous renin to plasma. To evaluate the hypothesis that suppressed plasma renin activity (PRA) in patients with low renin essential hypertension may be related to an alteration of the kinetics of the in vitro renin reaction, PRR was compared in plasma of patients with low renin and normal renin essential hypertension. Prostaglandin A (PGA) inhibits renin, and PGA was also measured to determine if suppressed PRA may be related to increased PGA. Low renin and normal renin hypertension were defined by comparing PRA responses of 30 hypertensive patients and 16 matched control subjects to upright posture and furosemide (80 mg p.o.). Nine of 30 patients had low PRA. Compared to that in plasma of patients with normal renin hypertension, PRR was suppressed (P less than 0.005) during 30, 60, and 180 min incubations in the low renin patients. Overall, in the hypertensive patients, there was a significant positive correlation (r= +0.58; P less than 0.01) between PRR and the PRA response to furosemide. PGA in patients with low renin hypertension (0.86 ng/ml+/-0.06 SE) was less (P less than 0.05) than that in patients with normal renin hypertension (1.10 ng/ml+/-0.07) SE) and control subjects (1.18 ng/ml+/-0.10 SE); PGA of normal renin patients and control subjects did not differ (P less than 0.1). These results suggest that an alteration of the kinetics of the renin reaction may contribute to the apparent renin suppression in patients with low renin hypertension. Hypertensive patients with suppressed PRA also have low PGA.
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PMID:Renin reactivity in plasma of patients with normal renin and low renin essential hypertension. 83 42

Prostaglandins are currently used to maintain patency of the ductus arteriosus and to elicit uterine contractions. Prostaglandin synthesis inhibitors are used to promote closure of the ductus and their administration in pregnant animals has produced fetal pulmonary hypertension. Exposure of the human fetus to inhibitors of prostaglandin synthesis has been associated with persistent pulmonary hypertension. A case report of a child with primary hypertension supports the hypothesis that the balance of prostaglandin metabolites plays an important role in maintaining PVR. Leukotrienes have been identified in the sputum of allergic asthmatic patients, patients with cystic fibrosis and infants with persistent pulmonary hypertension. Leukotriene inhibition in rats and newborn lambs prevented and reversed HPV. Receptors for prostaglandins have been identified in smooth muscle preparations of the uterus and renal glomerulus. Further studies have characterized the binding sites in lung tissue, giving supportive evidence for the existence of receptor sites there. Specific receptor sites for LTC4 and LTD4 have been demonstrated in lung tissue. Temperature, pH, and the presence of cations and guanine nucleotides have been shown to affect the receptor density and affinity. Lewis et al demonstrated that the characteristics of the receptor for [3H]LTD4 in the human lung are identical in adult and fetal tissue. This leads to the need for further investigation of the receptors and the effects of the local environments in an attempt to explain the physiologic changes seen in the successful and unsuccessful transition from fetal to neonatal circulation.
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PMID:Prostaglandin and leukotriene receptors in pulmonary, vascular, and uterine smooth muscle. 303 20

In normotensive and hypertensive humans, prostaglandins, particularly PGE2 and PGI2, affect blood pressure through control of vascular resistance, salt excretion, cardiac output, and renin secretion. The majority of studies of human essential hypertension have documented diminished renal synthesis and, hence, urinary excretion of PGE2. The acute administration of indomethacin inhibits prostaglandin synthesis and increases total peripheral resistance as well as mean blood pressure, with a countervailing decrease of cardiac index. The important vasodilatory and natriuretic roles of PGE2 and PGI2 are most apparent in hypertensive patients receiving antihypertensive therapy. The concomitant use of NSAID attenuates blood-pressure control in all reported studies using indomethacin. Consequently, potent NSAID should be avoided during treatment of hypertensive patients, and aspirin may be the safest NSAID in these circumstances. Interesting data are accumulating on the beneficial effects of polyunsaturated fatty acids, particularly linoleic acid and eicosapentaenoic acid, as dietary means to reduce blood pressure. All reported studies have documented small 5 to 10 mm Hg decrements of blood pressure with dietary supplementation with these fatty acids and conversion of the ratio of polyunsaturated to saturated fatty acids toward unity.
Adv Prostaglandin Thromboxane Leukot Res 1985
PMID:The relevance of prostaglandins in human hypertension. 315

Plasma 6-Keto-Prostaglandin F1 alpha (6-Keto PG F1 alpha; stable hydrolysis product of prostacyclin) levels in 24 patients with essential hypertension and 15 age and sex matched healthy controls were studied. 6-Keto PG F1 alpha levels were measured in extracted plasma by radioimmunoassay using a commercial kit. The 6-Keto PG F1 alpha levels were significantly (P less than 0.001) higher in hypertensive patients as compared to controls. The raised levels of plasma 6-Keto PG F1 alpha in hypertensive patients may be an adaptive response of blood vessels to increased blood pressure.
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PMID:Prostacyclin in (extracted) plasma of essential hypertensives. 330 Jan 16

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

Prostaglandins are naturally occurring compounds which are easily separable from other biologically active substances because of its acidic lipid nature. They are divided into 4 series, the A, B, E, and Falpha series, which differ in the structure of the characteristic 5-membered ring. Prostaglandins play a role in the following reproductive functions: 1) conception; 2) luteolysis; 3) menstruation; and 4) parturition. It has also been proposed that Prostaglandin A may be the natriuretic hormone, the circulating hormone which controls sodium reabsorption by the kidney. The experiments of Lee and Ferguson in which prostaglandins inhibited PAH uptake by rabbit renal cortex slices in vitro support this view. Prostaglandins are also implicated 1) in the fluid transfer in the gut; 2) as causative agents of diarrhea that accompanies medullary carcinoma of the thyroid or neural crest tumors; 3) in reducing blood pressure in humans with essential hypertension; 4) in fatty acid metabolism, including lipolysis; and 5) as mediators of the inflammatory response. Further research in prostaglandins will establish the validity of the proposed physiologic or pathologic functions of prostaglandins.
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PMID:Functions of prostaglandins. 458 48

The effect of bumetanide on absolute and fractional sodium excretion, creatinine clearance, and plasma renin activity (PRA) was studied in eight patients with essential hypertension before and after indomethacin. After bumetanide, urinary sodium excretion increased only in the first 4 hr, creatinine clearance only in the first 2 hr, and PRA rose progressively. After indomethacin, bumetanide caused a smaller increase in urinary sodium excretion, decreased creatinine clearance, and caused a small early and late PRA rise. Prostaglandin inhibition and indomethacin did not, per se, affect the tubular natriuretic mechanism but they abolished both early vascular and sustained PRA-stimulating effects of bumetanide.
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PMID:Influence of indomethacin on the natriuretic and renin-stimulating effect of bumetanide in essential hypertension. 700 29