Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to investigate the urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), thromboxane B2 (TxB2; a stable metabolite of TxA2), and PGE2 in 18 normal subjects, 49 cirrhotics with ascites without renal failure (GFR = 90 +/- 4 ml/min, means +/- S.E.M.) and 20 cirrhotics with functional renal failure (FRF) (GFR = 36 +/- 3). The study was made after 5 days on a 50 mEq sodium diet and without diuretics. Plasma renin activity (PRA), plasma norepinephrine concentration (NE) and plasma antidiuretic hormone concentration (ADH) were also measured. Cirrhotics without FRF showed a significantly higher urinary excretion of 6-keto-PGF1 alpha, TxB2 and PGE, (15.9 +/- 1.7 ng/h, 3.0 +/- 0.3 ng/h, and 6.2 +/- 1.0 ng/h) than did normal subjects (9.2 +/- 0.9, 1.3 +/- 0.1 and 2.3 +/- 0.4). On the contrary, the urinary excretion of these prostaglandins was normal or reduced in patients with FRF (5.3 +/- 0.8, 1.3 +/- 0.2 and 1.9 +/- 0.4). PRA, NE and ADH were significantly increased in cirrhotics with FRF (15.2 +/- 3.9 ng/ml/h, 1026 +/- 149 pg/ml and 4.1 +/- 0.3 pg/ml) and in patients without FRF (8.0 +/- 1.4, 667 +/- 67 and 3.9 +/- 0.3) as compared to normal controls (1.3 +/- 0.2, 275 +/- 46 and 2.4 +/- 0.2). These results suggest that renal hemodynamics in cirrhosis depends upon a critical equilibrium between the activity of endogenous vasoconstrictor systems and the renal production of the vasodilator prostaglandins PGI2 and PGE2. In addition, they do not support FRF in cirrhosis being related to an increased renal production of the vasoconstrictor prostaglandin TxA2.
...
PMID:Urinary excretion of 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in cirrhosis with ascites. Relationship to functional renal failure (hepatorenal syndrome). 346 43

The effect of dietary protein on the renin-angiotensin system was studied in rats. Rats were fed isocaloric, 50% (high protein, HP), or 6% (low protein, LP) protein diets with identical electrolyte content for 10 days. Food intake and electrolyte excretion were equivalent on the two diets. Plasma renin activity (PRA) was higher in HP (10.0 +/- 2.5 vs. 3.5 +/- 0.5 ng ANG I . ml-1 . h-1, P less than 0.02) as was plasma aldosterone. However, in conscious rats mean arterial pressure (MAP) was not different between groups. The pressor response to graded doses of angiotensin II (ANG II) was diminished by 30-60% with HP (all doses, P less than 0.05). ANG II binding by mesenteric artery smooth muscle particles did not differ between HP and LP. Chronic administration of captopril did not normalize the pressor response in HP. Urinary prostaglandin (PG) E and 6-keto-PGF1 alpha excretion was markedly increased by the HP diet. Acute inhibition of prostaglandin synthesis with meclofenamate restored the pressor response to ANG II in HP to that in LP. In summary, a HP diet increased PRA, plasma aldosterone, urinary PGE, and 6-keto-PGF1 alpha and decreased pressor responsiveness to ANG II. Resistance to ANG II was not reversed by chronic converting enzyme inhibition but was abolished by inhibition of prostaglandin synthesis.
...
PMID:Dietary protein increases plasma renin and reduces pressor reactivity to angiotensin II. 352 65

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.
...
PMID:Haemodynamic and endocrine responses of the kidney to frusemide in mild essential hypertension. 388 Dec 8

(a) Hemorrhage in dogs (to 45-50 mm Hg) was associated with a 10-fold increase in plasma renin activity (PRA) which remained elevated throughout the time-course of shock including the irreversible (decompensation) stage. The presence of angiotensin II (AII) in arterial blood was demonstrated by the bloodbathed organ technique and confirmed by blockade with specific AII antagonists (cysteine(8)-AII or isoleucine(8)-AII). The contribution of AII to systemic peripheral resistance during hemorrhage shock in dogs was established by administering AII antagonists which immediately cause a further fall in blood pressure.(b) Plasma catecholamines (CA) steadily increased during hemorrhage and peaked during compensation (a 100-fold increase). The CA decreased progressively during decompensation.(c) Prostaglandin (PG) E-like material was observed in arterial blood for 15-60 min (after hemorrhage); the peak arterial concentration was 2.6 ng/ml blood. Indomethacin (i.v., before 80% of maximum bleedout): (i) confirmed the presence of PGE, (ii) increased blood pressure, and (iii) increased blood loss.(d) Thus: peripheral resistance during hemorrhagic shock seems temporally correlated with blood CA levels (and not PRA), and the renin-AII system contributes to the maintenance of vascular resistance and may markedly decrease perfusion of organs, such as kidney; the administration of the proper combination of specific antagonists of vasoconstrictor humoral substances may radically improve organ perfusion and could contribute to ultimate recovery from hemorrhagic shock.
...
PMID:Profile of circulating vasoactive substances in hemorrhagic shock and their pharmacologic manipulation. 437 50

Recently several reports have been presented stating that glandular kallikrein is present in human and animal blood, and that the oral administration of hog pancreatic kallikrein (HPK) normalises decreased urinary kallikrein and prostaglandin E2 (PGE2) excretions and elevated blood pressure in hypertensive patients. In this study, HPK (2,000 KU/kg body weight) was intramuscularly injected into male rabbits, and several hormones (plasma kinins, plasma PGE, plasma 6-keto PGF1 alpha, plasma thromboxane B2 (TXB2), plasma renin activity (PRA), plasma aldosterone, plasma ACTH) were measured before and after HPK administration in order to clarify the role of glandular kallikrein in the blood. Plasma kinins concentrations were significantly increased (the mean baseline level: 1 +/- 1 pg/ml (mean +/- S.E.), 30 min: 230 +/- 22 (p less than 0.001), 60 min: 288 +/- 36 (p less than 0.001), and 120 min: 130 +/- 9 (p less than 0.001] after HPK administration. Plasma levels of PGE were slightly increased after HPK administration, but the change was not significant as compared with the mean baseline level. Plasma levels of 6-keto PGF1 alpha were significantly increased from the mean baseline level of 229 +/- 38 pg/ml to 594 +/- 131 (p less than 0.05) at 30 min and to 378 +/- 67 (p less than 0.01) at 60 min but were decreased to 278 +/- 37 at 120 min after HPK administration. On the other hand, the changes in plasma TXB2, aldosterone and ACTH concentrations, and PRA were not significant before and after HPK administration. From the present study, it was clarified that the exogenous intramuscular administration of HPK increased plasma levels of kinins and PGI2, but induced no elevation in plasma levels of other hormones including PRA. Therefore, it was concluded in this acute experiment that there was a close relationship between the kallikrein-kinin system and PGs.
...
PMID:[The effects of hog pancreatic kallikrein on the plasma kinins-prostaglandins and renin-angiotensin-aldosterone systems]. 609 84

Plasma renin activity, total renin, active renin, and aldosterone were measured as well as urinary prostaglandin E2 and kallikrein in a group of patients with hyperkalemia (6.1-7.7 mEq per liter) and hyporeninemic hypoaldosteronism. Plasma renin activity and aldosterone were low and the response was markedly blunted to upright posture, and furosemide. The rise in cortisol but not aldosterone was normal following ACTH stimulation. Active renin was depressed; however, total renin was normal. Urine PGE was variable including some low values, but the mean of the group was normal (p greater than 0.1). Urine kallikrein excretion was markedly diminished and undetectable in most cases. Fludrocortisone normalized potassium but minimally increased kallikrein in the patients. The possibility exists that kallikrein deficiency in these patients may underlie the inability to generate active renin.
...
PMID:Studies of the renal vasoactive systems in hyporeninemic hypoaldosteronism. 626 37

To ascertain whether renal prostaglandin (PG) E synthesis is decreased in patients with essential hypertension (EH), urinary PGE excretion (UPGEV) was measured in 47 normal females and 62 female patients with EH. In order to avoid contaminations of urine by seminal fluids, only female subjects were studied. UPGEV was also measured in female patients with renovascular hypertension (RVH) as well as primary aldosteronism (PA) or idiopathic hyperaldosteronism (IHA). As a whole, UPGEV was lower in patients with EH (226.9 +/- 13.7 ng/day) than that in normal females (317.3 +/- 22.1 ng/day, p less than 0.001). Younger patients (15 to 39 years) had significantly lower UPGEV than normal females of corresponding ages. However, there was no significant difference in UPGEV between older patients (over 40 years) with EH and normal females of the same age range. There were no significant differences in UPGEV among patients with low renin EH, normal renin EH, RVH, PA and IHA. We reconfirmed the decrease in UPGEV in patients with EH as compared with normal controls by studying female subjects. Further, it is suggested that renal PGE synthesis is not influenced by the renin-angiotensin system in these hypertensive states.
...
PMID:Reduced urinary excretion of prostaglandin E in essential hypertension. 634 5

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.
...
PMID:Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure. 637 Apr 31

Renal arterial infusion of acetylcholine (ACh) (40 micrograms/min) produces a natriuresis, diuresis, and an increase in renal plasma flow (RPF) without a change in glomerular filtration rate (GFR) or renin secretory rate (RSR). The present study was designed to examine the role of prostaglandins in this natriuretic response to ACh. In dogs pretreated with indomethacin (Indo) (5 mg/kg, i.v.), an inhibitor of prostaglandin synthesis, renal arterial infusion of ACh produced an increase and then a decline in urinary flow and sodium excretion accompanied by a progressive fall in GFR and RPF and a progressive increase in RSR. Renal arterial infusion of PGE2 (1.9 micrograms/min) but not PGF2 alpha (1.9 micrograms/min) before and during the infusion of ACh restored the diuretic and natriuretic response to ACh in Indo-treated dogs. Renal arterial infusion of bradykinin (BK) (3 micrograms/min) in Indo-treated dogs produced a diuresis and natriuresis similar to that produced by PGE2; renal arterial infusion of BK, however, did not restore the diuretic and natriuretic response to ACh in Indo-treated dogs. The data suggest that Indo shortens the diuretic and natriuretic response to ACh by inhibiting synthesis of prostaglandins, possibly PGE but not PGF. The data further suggest that PGE2 restores the diuretic and natriuretic response to ACh in Indo-treated dogs through a specific action rather than by its action as a renal vasodilator.
...
PMID:Prostaglandin E2 but not F2 alpha restores the natriuretic response to acetylcholine in indomethacin-treated dogs. 637 23

In eight normotensive male volunteers indomethacin decreased both the peak urine flow rate and total sodium excreted within 1 h of an intravenous dose of frusemide. Resting effective renal plasma flow and glomerular filtration rate were unchanged by indomethacin, but the increase in both parameters after frusemide was inhibited. The early increase in plasma renin activity after frusemide was inhibited by indomethacin. Indomethacin decreased urinary excretion of PGE by 80% and the increase after frusemide was abolished. The urinary excretion of a metabolite of systemic PGI2 was unaltered in the 40-60 min period following frusemide. The early haemodynamic effects of frusemide are likely to be prostaglandin mediated, but there was no evidence of any change in systemic PGI2 synthesis after frusemide.
...
PMID:Contribution of prostaglandins to the systemic and renal vascular response to frusemide in normal man. 642 43


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

---