Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CA levels, PRA, PAC responses to low and high sodium dialysates in haemodialysed patients were investigated. Increased levels of dopamine (DA), adrenaline (A) and noradrenaline (NA) were found during dialysis and ultrafiltration with high sodium dialysate (148 mEq/l), and significantly higher PRA with low sodium dialysate (131 mEq/l). PAC slightly but significantly decreased during dialysis with low sodium dialysate and significantly increased during ultrafiltration. The present results suggest that sodium dialysate concentration has a significant influence on the function of the autonomic system, PRA and PAC in haemodialysed patients.
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PMID:High and low sodium acetate haemodialysis and ultrafiltration. II. Comparison of plasma renin activity (PRA), catecholamine levels (CA) and plasma aldosterone concentration (PAC). 353 26

Sixteen patients (11 M, 5 F), median age 41 years, with essential hypertension insufficiently controlled on hydrochlorothiazide 75 mg/day (DBP greater than or equal to 100 mmHg) were investigated. Plasma renin concentration (PRC), angiotensin II concentration (PA II), aldosterone concentration (PAC), plasma noradrenaline concentration (PNAC), plasma volume (PV) and exchangeable sodium (NaE) were determined and a saralasin-infusion (5.4 nmol/kg/min) was carried out while the patients were on thiazide alone, and in fourteen cases, repeated 3 months later after addition of a beta-blocker (propranolol 6, metoprolol 6 and atenolol 2 patients). On thiazide alone PRC, PA II and PAC was higher than normal in the group as a whole and the angiotensin II-inhibitor, saralasin, caused a significant decrease in MAP in twelve out of sixteen patients. After addition of a beta-blocker SBP and DBP decreased from 164/109 mmHg to 136/94 mmHg. PRC and PA II decreased by 40% and 58%, respectively. At this point saralasin caused no significant change in MAP. No close correlation was found between changes in BP on beta-blocker treatment and either PRC, PA II or saralasin response on thiazide treatment. PV, NaE, PAC and PNAC did not change sigificantly. It is concluded that in pts with thiazide-induced stimulation of the renin-angiotensin system (RAS) addition of a beta-blocker leads to suppression of RAS and the angiotensin II dependence of the blood pressure is nearly abolished. This mechanism might well contribute to the antihypertensive effect of beta-blockade in this particular situation. However, the pharmacological changes induced by beta-blockade are very complex, and most likely other factors are involved in the antihypertensive effect of beta-blocking drugs.
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PMID:Angiotensin II blockade during combined thiazide-beta-blocker treatment. 610 82

Vitamin D3 was determined in commercially fortified instant nonfat dried milk by using normal phase high pressure liquid chromatography (HPLC). The sample was extracted with dichloromethane with sodium phosphate tribasic solution added. The sample was cleaned up by using a Sep-Pak silica cartridge and then a microparticulate column containing 10 micrometer Partisil-10 PAC packing material. The final analysis was performed by using a normal phase HPLC system with 10 micrometer LiChrosorb NH2 column. Recovery of vitamin D3 at levels as low as 10000 IU/kg was 97.7% with a standard deviation of 3.9%.
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PMID:High pressure liquid chromatographic determination of vitamin D3 in instant nonfat dried milk. 625 Oct 24

The new angiotensin converting enzyme inhibitor enalapril maleate was given in single oral doses of 2.5, 5, and 10 mg to 11 hospitalized patients with uncomplicated essential hypertension who were on a 150-mEq sodium diet. All doses of enalapril induced reduction of mean seated diastolic blood pressure (SDBP). The magnitude of the initial SDBP reduction was not dose related, but the duration of effect was longer (greater than 12 hr) after the 5 and 10 mg. After dosing, mean plasma angiotensin converting enzyme activity (ACE) and aldosterone concentration (PAC) fell, while plasma renin activity (PRA) rose. Serum concentrations of the active diacid from of enalapril increased linearly with dosage; ACE was inhibited maximally at concentrations above 10 ng/ml. During repeated dosing in the outpatient trial there was attenuation of the antihypertensive effect (12 to 24 hr after dosing) in eight of 10 patients. Despite dose increases only two patients achieved SDBP control (less than or equal to 90 mm Hg). In the five patients in whom 50 mg/day hydrochlorothiazide was added near the end of the trail mean SDBP was further reduced. Enalapril was well tolerated. Further studies of the drug, especially in combination with diuretic, are needed.
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PMID:Effects of enalapril, a new converting enzyme inhibitor, in hypertension. 628 27

We compared the effects of 500 ml of 0.15M NaCl or 750 ml of 0.15M NaHCO2, infusions on PRA and PAC in 16 normal NaCl-restricted men. More positive sodium balance, greater natriuresis, and lower serum chloride, potassium, and hydrogen ion concentrations were observed after NaHCO3 infusion. PRA decreased (13.8 +/- 1.0 ng/ml angiotensin I per hour to 6.6 +/- 0.70) and PAC did not change (98 +/- 15 ng/dl to 86 +/- 15) after NaCl infusion. Conversely, PRA did not change (9.9 +/- 1.6 to 10.1 +/- 1.6) and PAC decreased (85 +/- 9 to 44 +/- 5) after NaHCO3 infusion. Plasma cortisol declined in both groups. These results suggest that in sodium-restricted man chloride is more important than sodium for the suppression of PRA by NaCl loading and that potassium or hydrogen ion is a more sensitive modulator of aldosterone secretion than is renin.
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PMID:Renin and aldosterone responses to short-term NaCl or NaHCO3 loading in man. 628 47

Continuous ambulatory peritoneal dialysis (CAPD) entails the continuous presence of hypertonic dialysate in the peritoneal cavity. We postulated that the continuous, gradual ultrafiltration produces chronic activation of the renin-angiotensin system and the adrenal zona glomerulosa. To explore this hypothesis, we measured plasma levels of PRA, active renin (AR), total renin (TR), inactive renin (IR), 18-hydroxycorticosterone (18-OH-B), and aldosterone (PAC) under basal and stimulated conditions. At 0800 and 1200 hr after overnight recumbency, plasma levels of PRA, AR, TR, IR, and 18-OH-B were elevated above the range for sodium-replete recumbent normal subjects. PAC, however, was normal. The increase in TR was due predominantly to an increase in AR. After the combined stimulus of 4 hr ambulation and the ultrafiltration induced by a 2 L exchange, plasma levels of PRA, AR, TR, IR, and PAC were within the range for sodium-replete upright normal subjects. Plasma 18-OH-B levels, however, remained markedly elevated. Graded intravenous infusion of ACTH at rates of 0.03 to 10 ng/min demonstrated that the threshold for an ACTH-stimulated rise in plasma 18-OH-B and PAC is at least as low as that for cortisol and corticosterone. We conclude that CAPD produces activation of the renin-angiotensin system. The high circulating levels of PRA, AR, and, presumably, angiotensin II result in increased secretion of 18-OH-B by the adrenal zona glomerulosa.
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PMID:Plasma 18-hydroxycorticosterone during continuous ambulatory peritoneal dialysis. 631 27

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.
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PMID:Prostaglandins, renin, aldosterone, and catecholamines in preeclampsia. 636 75

In this multicenter study a nonnarcotic analgesic available for moderate pain, naproxen sodium, 550 mg, was compared to a combination that is used extensively for moderate to severe pain, aspirin, phenacetin, caffeine and codeine phosphate (APC/C) (60 mg of codeine phosphate). Women with pain after major gynecologic surgery reported a similar pattern in pain reduction with the two medications except for a relatively sharper increase in pain intensity between four and six hours after administration of APC/C. A smaller number of patient complaints suggested that naproxen sodium was better tolerated than APC/C.
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PMID:Naproxen sodium vs. a combination of aspirin, phenacetin, caffeine and codeine phosphate for pain after major gynecologic surgery. A multicenter comparison. 637 36

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.
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PMID:Prostaglandins, catecholamines, renin and aldosterone during hypertensive and normotensive pregnancy. 675 44

Autonomic neuropathy is one of the complications of diabetes, and several lines of evidence, supporting that sympathetic neural dysfunction may play the major role in the orthostatic hypotension (OH) of diabetic patients have been presented. In this paper the responses of plasma norepinephrine (PNE), plasma renin activity (PRA) and plasma aldosterone (PAC) to upright standing were studied in 17 diabetic patients without OH, 25 diabetics with OH and 17 age-matched, non-diabetic normotensives (controls). All were kept on a 200mEq sodium diet. Assay procedure for PNE was high-performance liquid chromatography with trihydroxyindol method and fluorimetric detection using dihydroxybenzylamine as internal standard. Intra- and inter-assay coefficient variations by this method were 3.4 and 5.8% respectively. PRA and PAC were determined by radioimmunoassay. Total blood volume was examined by the plasma tracer method using 131I-HSA and expressed in percent normal. Mean PNE level in the non-diabetic controls was 217 pg/ml in recumbency and increased to a level of 551 at 15 minutes on standing. The PNE responses to standing in the diabetic subjects without OH (defined as group I) were not significantly different from those in the controls. In the diabetics with OH, 14 cases, with the PNE increments less than 1SD below the mean in the controls, were defined as group III, and discriminated from other 11 subjects with OH (group II). PNE levels in group III were significantly lower than in the controls at both recumbency and upright posture. PRA was significantly elevated by standing in the controls and the diabetics except for group II. PRA in all the diabetic groups was significantly lower than in the controls, at both recumbent and upright. The mean values of PAC in the diabetics but group II at supine were significantly lower than those of the control group. PAC levels increased after standing contemporaneously with PRA, though significant rise in group II was shown without PRA response. Total blood volume was significantly (p less than 0.025) decreased in only group II. The results suggest: 1) PNE was normal in the diabetic patients without OH, 2) there are at least two types of OH in diabetes mellitus: one is hypoadrenergic and the other hypovolemic, 3) adrenergic neuropathy may be a cause of low PRA in diabetics with OH but another factor may also be involved in both with and without OH, 4) low PRA is a main factor of low PAC in diabetics (group I and III), but the dissociation between PRA and PAC responses to orthostasis is present in some cases (group II), which reflects disturbances in other regulatory mechanisms of aldosterone secretion.
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PMID:[The responses of norepinephrine, renin and aldosterone to standing in diabetic patients with orthostatic hypotension]. 675 61


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