Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When renal function is compromised, the circulation to the kidney is sustained by a major prostaglandin component, withdrawal of which results in significant hemodynamic effects, particularly reduction in blood flow to the inner cortex and medulla. Prostaglandins modulate the effects of vasoactive hormones by attenuating the renal actions of the renin-angiotensin system and contributing to and, perhaps, mediating some of those of the kallikreinkinin system. In addition, a prostaglandin mechanism, presumably located in the renal arterioles, participates in the regulation of renin release. Although cyclooxygenase is present in several renal tissues, the major products of arachidonic acid metabolism may be tissue specific and, consequently, their effects may be primarily restricted to one compartment, e.g., the proposed interaction of prostacyclin and renin within the vascular pole of the glomerulus; and PGE2/PGF2a with the kallikrein-kinin system within the urinary compartment. The former is related to the regulation of renin release and renal vascular resistance and the latter to the excretion of water and perhaps salt.
 ...
PMID:Compartmentalization of prostaglandins and prostacyclin within the kidney: implications for renal function. 10 56

Prostaglandins (PG) A1, B1, E2, F2 alpha and plasma renin activity (PRA) were measured by radioimmunoassay in 8 patients with unilateral artery stenosis, 7 hypertensive patients with unilateral renal atrophy without stenosis ans 20 controls. The measurement of the PG and PRA in the hypertensive group was performed in the infra-renal inferior vena cava and in the two renal veins. PRA and PGA1 were significantly raised in the renovascular hypertensive patients but no significant change was observed in the group with unilateral renal atrophy. On the other hand, the PGE2 and PGF2 alpha were raised in both groups, especially in the renal veins on the stenosed or atrophic side. There was a positive significant correlation between PRA and PGA1 and PGB, but none with PGE2 or PGF2 alpha. This study suggests that the increase in PGA1 and PGE2 represents a secondary hypertensive mechanism which is diuretic and natiuretic. The increase of PGF2 alpha represents a direct mechanism of hypertension. Simultaneous measurement of the vasopressor (PRA and PGF2 alpha) and vasodepressor (PGA and PGE) systems may give a better diagnostic and prognostic approach to renovascular hypertension.
 ...
PMID:[Prostaglandins in renovascular arterial hypertension]. 11 9

1. Prostaglandin E- and F-like material has been estimated in renal venous blood of the left kidney of anaesthetized rabbits following renal nerve section. Prostaglandins were estimated by bioassay following solvent extraction and column chromatography. 2. Electrical stimulation of the renal nerves of the left kidney to reduce renal blood flow by approximately 15% for 15 min resulted in a significant increase in the concentration of prostaglandin E-like material in the renal venous blood. The peak values were normally seen either in the last 5 min of the stimulation period or in the first 5 min after the end of the stimulation period. The concentration of prostaglandin F-like material was not significantly altered. 3. Similar reduction of renal blood flow of the left kidney by renal artery constriction also resulted in a significant increase in the concentration of prostaglandin E- but not F-like material in renal venous blood. The timing and magnitude of the response was comparable with that observed with renal nerve stimuation. 4. The effect of an angiotensin I converting enzyme inhibitor, SQ 20881, on the response to both renal nerve stimulation and renal artery constriction has been studied. The administration of the drug did not significantly reduce the release of prostaglandins from the denervated kidneys, however, the increase in prostaglandin E-like material, in response to both stimuli, was abolished. 5. The results suggest that the increase in prostaglandin E-like material released from the kidney in response to low frequency stimulation or to modest reductions in renal blood flow is dependent on the release of renin and that the effect is mediated by the formation of angiotensin II and not angiotensin I.
 ...
PMID:The effect of angiotensin I converting enzyme inhibitor (SQ 20881) on the release of prostaglandins by rabbit kidney, in vivo. 19 54

Urinary Prostaglandin E2 (PGE2), a known indicator of renal production, was measured by specific radioimmunoassay in 111 normal volunteers, 85 patients with essential hypertension, 6 with renovascular hypertension, and 23 patients with primary aldosteronism. Women excreted less PGE2 than men in both normotensive and hypertensive groups. When compared to normals, essential hypertensives demonstrated significantly lower PGE2 levels, with one third excreting less than 100 ng/24 hr, values usually seen only in subjects receiving the prostaglandin synthetase inhibitor, indomethacin. Normal PGE2 was seen in patients with renovascular hypertension, and levels were uninfluenced by treatment with the converting enzyme inhibitor SQ14225, Despite normalization of blood pressure and increased plasma renin activity. Normal PGE2 was also encountered in primary aldosteronism. These data indicate that impaired renal PGE2 biosynthesis is specific for human essential hypertension, and is not secondary to the elevated blood pressure. Although PGE2 excretion tends to be lower in low-renin hypertension, a constant relationship between PGE2 and renin is not always apparent.
 ...
PMID:Impaired renal prostaglandin E2 biosynthesis in human hypertensive states. 21 95

Two patients, one with Bartter's syndrome and one with severe abuse of diuretics, were investigated before and after indomethacin treatment. Before indomethacin the two patients showed a similar pattern of hypokalaemic alcalosis, secondary hyperaldosteronism, and increased urinary excretion of PGE2 and kallikrein. After a few days on peroral indomethacin medication the hypokalaemia was significantly improved, the plasma renin activity, and the urinary excretion of aldosterone, PGE2 and kallikrein were normalized in both patients. It is concluded that the beneficial effect of indomethacin cannot be used as a proof of prostaglandin overproduction as the primary defect in Bartter's syndrome.
 ...
PMID:On the pathogenetic role of prostaglandins in Bartter's syndrome. 28 69

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
 ...
PMID:Prostaglandins and the kidney. 33 46

We compared the ability of the vasodilator prostaglandins PGI2, PGE2, and 13,14-dihydro PGE2 to release renin when infused into the denervated, nonfiltering canine kidney in vivo. Papaverine was used as a nonprostaglandin vasodilator. All the prostaglandins tested were capable of stimulating renin secretion, with the scale of potency being 13,14-dihydro PGE2 greater than PGI2 greater than PGE2; papaverine had no effect on renin secretion. These results indicate that both PGE2 and PGI2 can stimulate renin secretion but that vasodilation per se is not a stimulus. 13,14-Dihydro PGE2 was included because it is a poorer substrate than PGE2, both for transport into cells and catabolism to inactive products, but has comparable potency to PGE2 when tested in systems with limited ability to catabolize PGE2. The fact that 13,14-dihydro PGE2 was the most potent prostaglandin tested suggests that the effects of PGE2 in our system are reduced by the kidneys' recognized ability to extract and catabolize PGE2. Since PGI2 is less avidly metabolized than PGE2 by the kidney, the differences in observed potency between PGE2 and PGI2 could be largely the result of differences in renal catabolism of the two prostaglandins rather than differences in intrinsic potency. Therefore, both PGE2 and PGI2 are candidates for the endogenous prostaglandin responsible for stimulating renin secretion.
 ...
PMID:Prostaglandins and renin release: the effect of PGI2, PGE2, and 13,14-dihydro PGE2 on the baroreceptor mechanism of renin release in the dog. 37 55

A detailed time course of changes in plasma renin activity (PRA), urinary prostaglandin (PG) E2, PGF2 alpha, thromboxane (TX) B2 and sodium excretion rates following furosemide was obtained in 7 women. PRA increased within the first 15 min and remained elevated all through the experiment. PGE2, PGF2 alpha, TXB2 and sodium increased simultaneously, reached a peak between 15 and 45 min after furosemide and declined thereafter. It is concluded that furosemide induces a generalized activation of the renal PG system temporally related to the increase of renin release and natriuresis.
 ...
PMID:Characterization of furosemide-induced activation of the renal prostaglandin system. 39 25

1. Urinary prostaglandins (PG), kallikrein and plasma renin activity (PRA) were measured in 35 patients with essential hypertension and 22 normotensive controls before and 15 min after frusemide (40 mg intravenously). 2. PGE2 and kallikrein excretion rates were lower in hypertensive subjects, and failed to rise to the same extent after frusemide. PGF2 alpha excretion was not significantly different in the two groups of patients either before or after frusemide. PRA rose less in the hypertensive subjects after frusemide. 3. These findings support the view that there is an abnormality of renal vasodilator systems (PGE2 and kallikrein) in essential hypertension.
 ...
PMID:Urinary prostaglandins and kallikrein in essential hypertension. 39 75

1. Urinary prostaglandin (PG) E2 excretion and plasma renin were measured in five healthy volunteer subjects for 2 h after intravenous injection of frusemid (protocol A) and during salt restriction for 7 days with frusemide added on the 2 last days (protocol B). 2 In protocol A, peak values in PGE2 and urine flow were reached in 10-20 min, after which the values rapidly subsided. Plasma renin increased twofold in 60 min. 3. In protocol B, even during severe antinatriuresis (day 5) and during maximal negative sodium balance (day 7), no change in urinary PGE2 excretion was observed. Plasma renin increased twofold on day 5 and increased tenfold on day 7. 4. The result of protocol B does not suggest any essential role of renal PGE2 for sodium excretion or sodium homeostasis in man. The result of protocol A may point to a role of renal prostaglandins for the diuretic action of frusemide.
 ...
PMID:Sodium balance, urinary prostaglandin E2 and renin in normal man. 39 76


1 2 3 4 5 6 7 8 9 10 Next >>