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

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.
Adv Prostaglandin Thromboxane Res 1976
PMID:Renal prostaglandins. 82 36

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

1. The hypothesis that suppression of prostaglandin E (PGE) synthesis by indomethacin exacerbates renal clip hypertension in the rat was investigated. 2. Indomethacin exacerbated hypertension in renal clip rats. 3. In vitro PGE synthesis determined by gas liquid chromatography (GLC) was suppressed in medullary tissue from the hypertensive animals irrespective of indomethacin treatment. 4. The findings support the concept that PGs participate in blood pressure regulation in experimental renal hypertension.
Adv Prostaglandin Thromboxane Res 1976
PMID:Renal prostaglandin synthesis in experimental renal clip hypertension in the rat. 98 62

The effect of prostaglandin E2 on the biosynthesis of corticosteroids was studied in intact rabbits and in the ones with vasorenal hypertension in different periods of its development (1st group) and in the animals subjected to a spurious operation (2nd group). Prostaglandin added to an incubation medium was found to produce in intact rabbits a significant depression of the 11-dehydrocorticosterone and cortisone biosynthesis from progesterone-C14. In rabbits operated upon (1st and 2nd groups) prostaglandin E2 brought changes in the production of corticosteroids no sooner than in 1 month after surgery. In rabbits with vasorenal hypertension brought about through unilateral constriction of the renal artery with an intact second kidney the content of the labeled 11-desoxycorticosterone and 11-desoxycorticosol materially decreased under the effect of prostaglandin E2, while the biosynthesis of the end fractions--11-desoxycorticosterone, aldosterone and cortisone, would gain in intensity. These changes preceded somewhat the most significant rise of the arterial pressure. In the rabbits spuriously operated upon prostaglandin E2 increased the production of corticosteroids and 11-dehydrocorticosterone, low at that time. It is presumed that prostaglandin E2 produces a regulating influence on the processes of the corticosteroids biosynthesis both in normalcy and in vasorenal hypertension.
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PMID:[Changes in the biosynthesis of corticosteroids from progesterone-C14 under the effect of prostaglandin E2 in rabbits with vasorenal hypertension]. 111 13

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

Prostaglandin and catecholamine concentrations were estimated in tumour tissues taken from four phaeochromcytomas and five other neural-crest tumours. Prostaglandins were found to be present in tumours both associated and non-associated with chronic diarrhoea. Prostaglandin F, as well as catecholamine, concentrations were higher in phaeochromocytomas than in other tumours. The hypothesis has been made that while prostaglandins do not reach arterial circulation to give rise to pharmacological effects, such as chronic diarrhoea, prostaglandins F present in phaeochromocytomas may contribute to a higher catecholamine synthesis and/or release, resulting in a higher incidence of hypertension associated with these tumours.
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PMID:Prostaglandins in neural crest-tumors. 119 79

These studies, using in vivo micropuncture techniques in the Munich-Wistar rat, document the magnitude of changes in glomerular and tubular function and structure 24 h after approximately 75% nephron loss (Nx) and compared these results with those obtained in sham-operated rats. The contribution of either nephron hypertrophy or renal prostaglandin to these adjustments in nephron function was also explored. After acute Nx, single nephron GFR (SNGFR) was increased, on average by approximately 30%, due primarily to glomerular hyperperfusion and hypertension. The approximately 45% reduction in preglomerular and the constancy in postglomerular vascular resistances was entirely responsible for these adaptations. Although increases in fluid reabsorption in proximal convoluted tubules correlated closely with increase in SNGFR, the fractional fluid reabsorption between late proximal and early distal tubular segments was depressed. Nephron hypertrophy could not be substantiated based on either measurements of protein content in renal tissue homogenates or morphometric analysis of proximal convoluted tubules. However, acute Nx was associated with increased urinary excretory rates per functional nephron for 6-keto-PGF1 alpha and TXB2. Prostaglandin synthesis inhibition did not affect function in control nephrons, but this maneuver was associated with normalization of glomerular and tubular function in remnant nephrons. The results suggest that enhanced synthesis of cyclooxygenase-dependent products is one of the earliest responses to Nx, and even before hypertrophy the pathophysiologic effects of prostaglandin may be important contributors to the adaptations in remnant nephron function.
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PMID:Glomerular and tubular adaptive responses to acute nephron loss in the rat. Effect of prostaglandin synthesis inhibition. 169 76

The origin of pre-eclampsia lies in uteroplacental ischemia due to an anomaly of the "vascular insertion" of the placenta. Although the cause of this anomaly remains unknown, it would appear to include both a genetic and an immunological origin possibly favourised by special underlying conditions and certain obstetric circumstances. Prostaglandin imbalance (in particular prostacyclins and Thromboxane A2) appears to be one of the chief factors governing these anomalies. One of the consequences of these mechanisms is the onset of hypertension but other disturbances are essential features. In particular, disseminated intravascular coagulation may occur leading to the release of numerous microthrombi which cause placental (leading to chronic fetal distress), renal, hepatic and cerebral lesions.
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PMID:[Physiopathological elements of pre-eclampsia and the role of the main complementary tests]. 176 67

Prostaglandin (PG) E2 receptor-adenylate cyclase system was studied in the kidney of 12-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to evaluate the role of this system in hypertension. PGE2 receptors were determined by a radioligand binding method using [3H]-PGE2. Adenylate cyclase responses to PGE2, sodium fluoride (NaF) and forskolin were also measured. The concentration of PGE2 receptor was increased in SHR compared with WKY. PGE2- and NaF-stimulated adenylate cyclase activities were significantly lower in SHR than WKY. There was no significant difference in forskolin-stimulated adenylate cyclase activity between SHR and WKY. NaF activates the nucleotide binding regulatory protein (G-protein) and forskolin directly activates the catalytic unit. These results indicate that the activity of G-protein coupled with renal PGE2 receptors is deficient in SHR. This defect may contribute to the elevation of blood pressure, through sodium retention.
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PMID:Deficient activity of nucleotide binding regulatory protein coupled with PGE2 receptor in renal medulla of spontaneously hypertensive rats. 210 7

An increased platelet-vessel wall interaction plays an important role in most forms of cardiovascular disease. In healthy arteries, the vascular endothelium prevents platelet adhesion and aggregation. As a mediator of this protective function, the endothelium produces prostacyclin, endothelium-derived nitric oxide and tissue plasminogen activator. Cardiovascular risk factors such as hypertension, hyperlipidemia and diabetes are associated with an increased platelet activation and with decreased antithrombotic properties of the blood vessel wall. The available inhibitors of platelet function interfere only with one of various mechanisms of platelet activation and of the platelet-vessel wall interaction. Prostaglandin inhibitors, such as aspirin and newer, more specific inhibitors, prevent the production and/or the effect of thromboxane A2 on platelets and the blood vessel wall. Other drugs interfere with the effect of adenosine diphosphate on platelets, or they increase intracellular concentration of cyclic GMP or AMP in platelets and vascular smooth muscle cells. The protective effects of platelet inhibitors in primary and particularly in secondary prevention of cardiovascular diseases have been documented in numerous studies. The successful clinical use of these substances, however, requires a selective prescription of the drugs in patients with cardiovascular disease.
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PMID:[Thrombocyte inhibitors in cardiovascular therapy]. 221 49


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