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)

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

Twenty patients with hypertension were studied under diets containing low and high salt to identify factors which might be involved in elevating blood pressure under sodium-loading. They were classified as "salt-sensitive" (SS) and "nonsalt-sensitive" (NSS) according to the presence or absence of greater than 10% increases in mean blood pressure when a low salt diet was replaced by a high salt diet. During high-sodium intake, the SS patients showed reduced urinary excretion of sodium and elevated plasma levels of aldosterone as compared with plasma renin activity. The SS patients also showed an enhanced pressor response to norepinephrine under both low-sodium and high-sodium diets. From these results, it is suggested that the sodium retention, which is probably related to nonsuppressed levels of PAC under sodium-loading, is one of the factors in elevating blood pressure in the SS patients. Moreover, the enhanced pressor response to norepinephrine seems to contribute, in part, to elevation of blood pressure in the SS patients under salt-loading.
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PMID:Enhanced vascular reactivity to norepinephrine in salt-sensitive patients with hypertension. 676 53

The studies were designed to explore the effect of the converting enzyme inhibitor captopril on the activity of the sympathetic nervous system during basal conditions and following graded physical exercise in patients with essential hypertension. Seven males and two females, aged 36-59 years, were hospitalized under metabolic ward conditions and treated for 7 days with captopril given orally in increasing dosages, the final dose being 600 mg daily. The patients were subjected to an individual, graded submaximal work test (bicycling) for 20 min before medication and then again in an identical manner during medication with 600 mg captopril. Blood samples were drawn before exercise and then after 10 and 20 min of work for the determination of plasma angiotensin II (PA II), plasma aldosterone (PAC), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma adrenaline (PA). Before medication blood pressure (mmHg) was 195/133 immediately before exercise, 230/129 after 10 min of moderate exercise and 263/105 following 20 mon of nearly maximal work. During treatment with captopril the respective blood pressure values were 154/110, 200/100 and 245/98. Captopril had no significant effect on the changes in heart rate following physical exercise. PA II and PAC were substantially reduced and PRA considerably increased by captopril. PA II, PAC and PRA increased in response to exercise both before and following captopril. The exercise stimulated increase in PNA and PA was almost identical before and during captopril. Thus, captopril had no major effect on the activity of the sympathetic nervous system in patients with essential hypertension, neither during basic conditions nor during heavy physical exercise in spite of a profound decrease in PA II.
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PMID:The effect of captopril on catecholamines, renin activity, angiotensin II and aldosterone in plasma during physical exercise in hypertensive patients. 680 Aug 10

The acute adrenal response to potassium chloride and angiotensin II (A II) infusions was studied in hypopituitary patients and compared with normal subjects. The peripheral plasma levels of aldosterone (PAC), cortisol (F), potassium (K), and plasma renin activity (PRA), were measured at 09.00 h and after 60 and 120 min of infusion. All subjects were recumbent ad under balance conditions, receiving a daily dietary intake of 180 mmol of sodium and 80 mmol of potassium. Basal PAC in hypopituitary patients was not significantly different from that observed in the control group. Both normal and hypopituitary patients respond to A II infusion with significant increments. Under potassium chloride stimulus the PAC response in hypopituitary patients was only observed when cortisol (20 mg) was given 2 h prior to the infusion. When cortisol replacement was omitted the response KCl was not detected. These results suggest a permissive role of cortisol on glomerulosa response to potassium.
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PMID:Plasma aldosterone response to angiotensin II and potassium chloride infusions in hypopituitary patients. 700 72

The role of the renin-angiotensin system in the control of aldosterone and other mineralocorticoids was studied in 9 hyperkalemic patients with chronic renal failure showing mild azotemia (group I) and 6 normokalemic patients with chronic renal failure showing creatinine clearance similar to that in group I (group II). In group I, the plasma renin activity (PRA) was significantly low and plasma aldosterone (PAC) and 18-hydroxycortisterone (18-OH-B) were also significantly reduced. In group II, PRA was normal or slightly increased, and PAC and 18-OH-B were also normal or slightly increased. Both the PAC and 18-OH-B in group I were stimulated by ACTH and angiotensin II, although the responses were less than those in group II. In 2 patients of group I where PRA moved into the normal range after administration of furosemide, the plasma 18-OH-B and PAC also reached the lower limit of normal. These results suggest that suppression of the renin-angiotensin system is probably related to functional disturbance in the conversion from B to 18-OH-B and/or 18-OH-B to aldosterone in most abnormally hyperkalemic patients with chronic renal failure.
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PMID:Renin, aldosterone and other mineralocorticoids in hyperkalemic patients with chronic renal failure showing mild azotemia. 703 83

To elucidate the significance of long-term administration of dexamethasone in order to differentiate the 4 types of hyperaldosteronism, blood pressure, serum electrolytes, plasma renin activity (PRA) and diurnal rhythm of plasma aldosterone (PAC) were studied before and after long-term dexamethasone (Dex) administration in patients with aldosterone-producing adenoma (APA), idiopathic hyper aldosteronism (IHA), unilateral adrenal hyperplasia (UAH) and Dex suppressible hyperaldosteronism (DSH). The results were as follows: 1) In APA with ACTH-dependent aldosterone secretion, long-term Dex administration induced a significant depression of PAC associated with an elevation in serum potassium (s-K). In almost all patients with APA, the diurnal rhythm of PAC, parallel to that of ACTH, completely disappeared following Dex administration. 2) In most patients with IHA, PAC was mainly influenced by the renin-angiotensin system. Dex did not affected on s-K, but it induced a slight decrease in PAC in some patients with IHA. 3) In UAH having similar pathophysiological findings of the adrenal cortex as IHA, Dex decreased PAC. 4) In DSH, Dex at a dose of 6 mg/day decreased PAC to normal value in association with normalization of blood pressure and s-K. From these results, hyperaldosteronism inducing a decrease in PAC and an increase in s-K by Dex is possibly diagnosed as APA, while the patients with no change of s-K by Dex may be diagnosed as IHA. Even if PAC is suppressed with Dex and ACTH-independent, the hyperaldosteronism may be UAH. It may be possible that factors other than aldosterone are important to induce hypokalemia in patients with IHA. Furthermore, it is suggested that UAH is a precedent pathophysiological condition of aldosterone-producing adenoma in the adrenal cortex. It is concluded that the measurement of s-K and diurnal rhythm of PAC before and after Dex administration are useful for discriminating APA and IHA.
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PMID:[The long-term administration of dexamethasone for the differentiation of the 4 types of hyperaldosteronism]. 775 Jun 27

The effects of a 7-day intraperitoneal infusion with VIP (0.03 nmol.kg-1.min-1) and its antagonist [4-Cl-D-Phe6,Leu17]-VIP (VIP-A; 3 nmol.kg-1.min-1) were studied in sham and bilaterally adrenalectomized rats bearing ACTH and angiotensin II (ANG-II)-responsive adrenocortical autotransplants. VIP significantly increased plasma aldosterone (ALDO) concentration (PAC) and lowered plasma renin activity (PRA) in both groups of animals, without affecting plasma levels of ACTH and corticosterone. This treatment caused a marked hypertrophy of adrenal zona glomerulosa (ZG) and its parenchymal cells (without inducing any significant change in the zona-fasciculata morphology), as well as of ZG-like cells of autotransplants. Isolated ZG cells and autotransplant quarters obtained from VIP-infused rats evidenced a notable increase in both their basal and maximally ACTH- or ANG-II-stimulated ALDO secretion. The simultaneous infusion of rats with VIP-A completely reversed all these effects of VIP. The infusion with VIP-A alone caused, in sham-operated rats, a net decrease in PAC, coupled with a rise in PRA, and a marked atrophy of ZG and ZG cells; basal and maximally stimulated ALDO secretion of dispersed ZG cells was also significantly lowered. Conversely, VIP-A did not evoke any appreciable effect in autotransplanted rats. These findings suggest that endogenous VIP is specifically involved in the maintenance of the growth and secretory capacity of rat adrenal ZG. Since regenerated adrenocortical autotransplants, which are responsive to VIP but not to VIP-A infusion, are completely deprived of chromaffin cells, the hypothesis is advanced that adrenal medulla may be the source of endogenous VIP regulating ZG function.
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PMID:Evidence that endogenous vasoactive intestinal peptide (VIP) plays a role in the maintenance of the growth and steroidogenic capacity of rat adrenal zona glomerulosa. 794 54

Cysteamine, a specific somatostatin depleter, was given to male rats to clarify its role in relation to the renin-angiotensin-aldosterone (RAA) axis and glomerulosa cell growth. Rats received seven daily sc injections of cysteamine at doses of 50 or 150 mg/kg body weight (BW). Their adrenal weights and whole cortical thickness increased, but zona glomerulosa thickness decreased dose-responsively. Plasma renin activity (PRA) and aldosterone concentration (PAC) decreased. Similar results were observed in rats on a low or high salt diet and receiving daily doses of 150 mg/kg BW of cysteamine. In hypophysectomized rats, however, cysteamine given for seven days at daily doses of 100 mg/kg BW did not change either PRA or PAC. Adrenal weight did not change either too. Our results indicate that cysteamine suppresses the RAA axis and glomerulosa cell growth, probably through pituitary factors.
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PMID:Effects of cysteamine, a somatostatin depleter, on the renin-angiotensin-aldosterone axis and glomerulosa cell growth in rats. 795 74

Recent studies have shown that both in hypertensives and in offspring of hypertensive parents there exists an altered renal functional reserve (RFR). The aim of this research was to study the RFR in newly diagnosed essential hypertensives, and to evaluate if any influences are played on RFR by circulating renin-angiotensin-aldosterone system, catecholamines, and plasma endothelin-1. In 16 essential hypertensives (EH) and in 10 healthy controls (C), on the 24-hour urine collection and on urine specimens taken after both an oral water load and an amino acids (AAs) infusion (4.16 ml/min for two hours), Ccr, microalbuminuria (AER) and its fractional clearance, and sodium excretion (Nau) were evaluated. Furthermore, both in basal condition and after the AAs load, blood samples were obtained to assay plasma renin activity (PRA) and aldosterone concentrations (PAC), circulating norepinephrine (NE) and endothelin-1 (ET-1). The C-group showed a mean increase in Ccr of 35%. No significant modifications in AER and in circulating hormones were observed. Among the 16 EH, thirteen subjects showed a significant increase in Ccr after the AAs load, with a mean increase of 32.5%. In the whole group of EH there were no significant differences in AER when comparing basal with after-load values, and Nau resulted significantly decreased after AAs infusion. The analysis of the hormonal pattern pointed out not significant changes in the behaviour of PRA, NE and ET-1, while a significant decrease in PAC was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The renal functional reserve in recently diagnosed essential hypertension. 802 14


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