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)

Among the subsets of LRA, IHA and GSA should always be treated medically. APA and APC should be treated surgically if possible, with unilateral adrenalectomy. First-line treatment of IHA and for preoperative preparation of APA and APC patients is the aldosterone antagonist spironolactone. If this agent cannot be used because of side effects, sodium transport inhibitors are appropriate alternatives. Patients with IHA and APA can also be treated with calcium channel blockers, but only nifedipine has been tested in these conditions. IHA can probably also be treated with the converting enzyme inhibitor enalapril, but the experience with this agent is very limited. The same is true for steroidogenesis inhibitors, of which ketoconazole seems to be the most promising. GSA is usually treated with dexamethasone. Spironolactone and amiloride can be used as alternatives. The only proven auxiliary medication for treatment of APC is o,p'-DDD.
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PMID:Medical treatment of low-renin aldosteronism. 266 81

In order to examine the relationship between the renin-aldosterone system and atrial natriuretic polypeptide (ANP), we investigated the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on the plasma concentrations of renin (PRC) and aldosterone (PAC), as well as the effects of captopril pretreatment on the natriuresis and blood pressure reduction induced by alpha-hANP in rats. Although alpha-hANP infused into conscious rats at 0.67 microgram min-1 kg-1 markedly increased the urinary excretion of sodium and decreased mean arterial pressure, its infusion did not change PRC; however, it significantly lowered PAC. Frusemide infusion at 20.8 micrograms min-1 kg-1 induced natriuresis comparable with that of alpha-hANP and it elevated both PRC and PAC, but mean arterial pressure was not altered. Pretreatment of rats with captopril did not have any significant influence on the acute natriuretic and hypotensive effects of alpha-hANP. Although the inhibitory effect of ANP on the renin-aldosterone system may be involved in the chronic modulation of body fluid volume and blood pressure, this effect does not seem to be directly involved in the acute natriuretic and hypotensive effects of the peptide.
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PMID:Relationship between the renin-aldosterone system and atrial natriuretic polypeptide in rats. 294 8

In 12 patients with essential hypertension who remained hypertensive despite chronic chlorthalidone treatment, the effect of 2 weeks of additional therapy with the converting enzyme inhibitor (CEI) enalapril on blood pressure and body fluid volumes has been evaluated. The objective was to examine the influence of a diuretic-stimulated renin-angiotensin-aldosterone system (RAAS) on haemodynamics and body fluid volume. Mean arterial pressure (MAP -21%), total peripheral resistance index (TPRI -22%) and plasma aldosterone concentration (PAC -39%) were decreased, and plasma renin activity (PRA 660%) was increased. The average heart rate (HR), cardiac index (CI), plasma volume (PV), blood volume (BV), extracellular fluid volume (ECFV) and body weight (BW) remained unchanged. A negative correlation was found between the per cent changes in ECFV and PAC. Thus, body fluid volumes during chronic diuretic treatment are well preserved even when the RAAS with its sodium retaining properties is suppressed by CEI. Possible mechanisms are a volume (not angiotensin II) - dependent stimulation of aldosterone and a fall in blood pressure.
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PMID:Changes in haemodynamics and body fluid volume due to enalapril in patients with essential hypertension on chronic diuretic therapy. 302 15

Aldosterone secretion in man is stimulated by potassium (K), ACTH, and angiotensin II (AII) and inhibited by dopamine (DA). In normal sodium-replete supine individuals, aldosterone secretion is under maximum tonic inhibition by DA and is not inhibited further by DA administration. Sodium depletion alters plasma aldosterone responses to secretogogues. Upright posture, another physiological stimulus to aldosterone secretion, recently was demonstrated to sensitize the adrenal cortex to inhibition of aldosterone secretion by a large quantity of DA (4.0 micrograms/kg X min). The effect of upright posture on aldosterone responses to other secretogogues is unknown. In this study, we investigated the effect of upright posture on aldosterone responses to low infusion rates of DA, to the DA antagonist metoclopramide (M) and to AII and ACTH. Fourteen normal men eating a normal sodium diet were studied. In eight, PRA, plasma aldosterone (PAC), plasma cortisol (F), and serum K concentrations were determined after 4 h of upright posture and infusion of vehicle (D5W) or DA at 0.1, 0.4, and 2.0 micrograms/kg X min. Six other normal men were kept supine for 3 h and, on separate days, upright for 3 h and given iv M (10-mg bolus dose), AII (1 and 4 pmol/kg X min for 30 min), and ACTH (20 and 120 mU/h for 30 min). PAC, PRA, F, and K were measured before and after these three secretogogues were administered. In the presence of vehicle, mean PAC increased by 15.1 +/- 4.3 (+/- SEM) ng/dL after 4 h of upright posture. In the presence of DA infused at 0.1, 0.4, and 2.0 micrograms/kg X min, the PAC response to upright posture was decreased to 9.7 +/- 2.5 (P = NS), 7.5 +/- 3.9 (P less than 0.05), and 8.1 +/- 2.0 (P less than 0.05) ng/dL, respectively. This occurred without a decrease in PRA, F, or K. The stimulation of PAC 10 and 20 min after a 10-mg bolus dose of M was 9.6 +/- 3.3 and 9.3 +/- 2.6 ng/dL, respectively, in supine subjects and 8.3 +/- 2.3 and 10.8 +/- 3.4 ng/dL 10 and 20 min after the M dose in upright subjects. The responses of PAC to ACTH and AII also were unchanged after 3 h of upright posture. We conclude that upright posture sensitizes the adrenal cortex to inhibition of aldosterone secretion by DA without affecting other modifiers of aldosterone secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of upright posture on the aldosterone responses to dopamine, metoclopramide, angiotensin II, and adrenocorticotropin. 303 55

To investigate the effects of dietary sodium on the peripheral dopaminergic mechanism, changes of unconjugated plasma dopamine(DA) and its related humoral factors were studied in 8 patients with essential hypertension(EH) and 8 age-matched normal controls(N) while they were receiving ordinary meals (Na, 130-180 mEq daily) followed by higher sodium (250-300 mEq daily) diets for a week. Plasma and urinary DA, norepinephrine(NE) and epinephrine(E) were measured by the highly sensitive COMT-mediated radioenzymatic procedure, which permits an accurate estimation of plasma DA as low as 5-6 pg/ml. Under high sodium diets, blood pressure and heart rate were not changed significantly in N and EH subjects. Urinary NE and E tended to decrease, while urinary DA increased significantly in both groups of subjects (p less than 0.05). There was a significant correlation between urinary sodium and DA (r = 0.590, p less than 0.001), but plasma DA failed to correlate significantly to urinary sodium or DA in all subjects. Plasma NE and E tended to decrease in both N and EH subjects, while plasma DA increased significantly (p less than 0.05) in EH from 7.2 +/- 0.8 pg/ml [mean +/- SEM] to 9.3 +/- 1.0 and slightly in N from 9.1 +/- 1.8 to 11.2 +/- 1.3. Plasma renin activity(PRA) and plasma aldosterone(PAC) were invariably decreased in all subjects, while plasma prolactin(PRL) remained unchanged. A significant correlation was observed between plasma DA and NE under ordinary meals (r = 0.733, p less than 0.01), but this correlation disappeared under high sodium diets. Plasma DA showed an inverse correlation to PAC (r = 0.351, p less than 0.05) under both dietary conditions. Upright posture induced a significant rise (p less than 0.05) in NE, E, DA, PRA and PAC with ordinary meals, but the responses of NE and PAC were apparently attenuated with high sodium diets. An intravenous injection of metoclopramide (MCP, 10 mg), a DA receptor antagonist, provoked a slight rise in plasma NE and DA with ordinary meals, of which responses were further enhanced with high sodium diets. MCP induced a definite rise in PAC and PRL in all subjects under both dietary conditions (p less than 0.01), while plasma E and PRA remained unchanged after MCP challenge. The results lend support to the view that unconjugated plasma DA could be a useful marker of peripheral dopaminergic activity, which might be a physiological regulator responsible for the suppression of aldosterone secretion and sympathetic nerve activity observed during high sodium intake.
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PMID:[Effects of high sodium diet on dopaminergic mechanism in normal and hypertensive subjects]. 306 95

Acute extracellular volume expansion (VE) by isotonic saline is associated with variable change in mean arterial pressure (MAP) in normotensive subjects (NT). Following VE by 1,800 ml isotonic saline in 3 h, two patterns of MAP response were observed in NT: either an increase by more than 10% (SS: sodium or VE sensitive, n = 12) or no change (NSS: non-sodium or VE sensitive, n = 14). We assessed in all subjects the response to VE of glomerular filtration rate (GFR), urinary sodium (UNaV) and kallikrein (UKalV) excretion rate, plasma renin activity (PRA) and aldosterone concentration (PAC). Family history of blood pressure was not different between the groups. In response to VE, MAP increased (88 +/- 3 to 102 +/- 4 mmHg) in group SS and did not change in group NSS (83 +/- 3 to 85 +/- 3 mmHg). Whilst UNaV measured during the hour prior to VE was similar in both groups, the total amount of sodium excreted during VE was higher in group SS than in group NSS (52 +/- 9 vs 32 +/- 3 mmol/3 h, p less than 0.05). Control GFR as well as changes in GFR associated with VE were similar in both groups. A similar decrease in PRA and PAC was observed in both groups and pre-VE values were identical. UKalV was lower in SS than NSS subjects during the pre-VE control jour (0.42 +/- 0.09 vs 0.74 nKat/h; p less than 0.05) and during VE (1.14 +/- 0.16 vs 2.5 vs 0.47 nKat/3 h; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary excretion of kallikrein and sensitivity of blood pressure to acute sodium loading in healthy subjects]. 309 97

The effect of feeding frequency and associated meal size on the renin-angiotensin-aldosterone system (RAAS) in seven horses was examined. A daily maintenance ration of hay-grain pellets was provided either as a multiple feeding regimen (MF), in which the ration was divided into six equal portions fed at 4-h intervals, or as a single large feeding (SF) given from 9 A.M. until 11 A.M. Plasma renin activity (PRA), aldosterone (PAC), cortisol (PCC), protein concentration (TP), packed cell volume (PCV), and serum sodium and potassium were measured serially. To prevent significant RAAS stimulation due to strenuous exercise or by assuming orthostatism after a period of recumbency, the horses were trained to stand in 1 X 4-m tie stalls during the experiments. Changes in Na intake were prevented by disallowing nonration salt sources. A 12:12 light-dark interval was maintained. During the MF experiment, only serum Na changed diurnally, with concentrations lowest in early morning and highest before midday. In contrast, during the SF experiment, PRA was increased at 0.5, 1.0, and 3.0 h and PAC was increased at 3.0, 5.0, and 7.0 h after onset of feeding (P less than 0.005). Increased TP and PCV suggested transient hypovolemia was responsible for renin release. Significant increases in Na and decreases in K occurred while eating; however, K increased postprandially to be coincident with aldosterone. Except for a transient increase during feeding in SF, PCC demonstrated a similar circadian rhythm in both experiments. It was concluded that 1) episodic feeding (SF) causes significant diurnal variation of the RAAS in the horse, and 2) spontaneous circadian activity of the RAAS cannot be demonstrated in this species during a steady-state feeding regimen (MF).
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PMID:Effect of feeding on renin-angiotensin-aldosterone system of the horse. 327 28

The validity of the captopril test for primary aldosteronism (PA) was tested in patients with surgically verified PA (n = 12) or essential hypertension (EHT, n = 20) with different levels of sodium intakes. The patients were scheduled on 7 days each of three regimes of the prepared diet containing 34, 120 and 340 mEq of sodium chloride per day, and the captopril test was repeated in each period. For the test, captopril (50 mg) was administered orally at 9:00 A.M. after 1 hour of rest in a supine position, and venous blood samples were obtained before and 90 min after drug administration. Plasma aldosterone concentration (PAC; ng/dl) and plasma renin activity (PRA; ng/ml/h) were measured by radioimmunoassay. Under the three different sodium intakes, a PAC/PRA ratio greater than 20 at 90 min after captopril administration was sufficiently sensitive (0.95, 19/20) and specific (0.92, 55/60) to identify PA. Similarly, PA was associated with a PAC above 15 ng/dl 90 min after captopril. There were no complaints associated with the antihypertensive effects of the drug even when patients were sodium-restricted. These results confirmed that the captopril test is safe and useful for screening out-patients for PA, independent of individual differences in sodium intake.
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PMID:Effects of sodium intake on the captopril test for primary aldosteronism. 330 11

Twelve women in their first 3 months of pregnancy received an i.v. saline load (3 mmol sodium/kg) and a graded infusion of angiotensin II (Ang II; i.e. 4, 8 and 16 ng/kg per min). As controls, twelve comparable pregnant subjects received the saline infusion alone. Eight non-pregnant women underwent both protocols, with doses of 2, 4 and 8 ng/kg per min Ang II, and thus acted as their own controls. Saline loading evoked proportionately similar falls in basal plasma renin (PRC) and plasma aldosterone (PAC) concentrations in pregnant and non-pregnant women. Angiotensin II evoked a dose-dependent pressor response, a graded increase in PAC and a reduction in sodium and urate excretion in both pregnant and non-pregnant women. The administration of Ang II had a proportionately greater effect on sodium and urate excretion in non-pregnant than in pregnant women; the pressor response to Ang II was also decreased in the pregnant women. The stimulation of PAC by Ang II, however, did not differ between the two groups. These results show that refractoriness to the renal and vascular effects of Ang II is present as early as the eleventh week of gestation. They also support the hypothesis that there is a degree of dissociation between the renin-angiotensin system and PAC in normal pregnancy.
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PMID:The effects of intravenous angiotensin II upon blood pressure and sodium and urate excretion in human pregnancy. 341 Nov 23

Aldosterone secretion in man is stimulated by potassium, ACTH, and angiotensin II and is inhibited by dopamine (DA). In normal sodium-replete supine individuals, aldosterone secretion is under maximum tonic inhibition by DA. Dopaminergic control of aldosterone secretion is modified by dietary sodium depletion. To determine the physiological significance of dopaminergic inhibition of aldosterone secretion, we studied the effect of DA on the aldosterone response to upright posture. Twelve normal men were studied while eating an ad libitum sodium diet, and the effect of DA was determined in the supine and upright positions. Plasma aldosterone (PAC), plasma cortisol (F), plasma aldosterone-stimulating factor (ASF), PRA, and blood pressure were measured while the men were supine and after 4 h of upright posture during an infusion of 5% dextrose vehicle and during a DA infusion of 4.0 micrograms/kg X min. The men also were studied as a time control in the supine position while receiving vehicle or DA. PAC increased from a mean basal value of 20.4 +/- 3.2 ng/dl (+/- SE) by 25.9 +/- 5.1 ng/dl to a peak of 44.4 +/- 2.4 ng/dl in response to upright posture during vehicle infusion. The PAC response to upright posture was reduced to 7.4 +/- 1.8 ng/dl (P less than 0.05) when DA was infused. The increase in PRA with upright posture was 3.7 +/- 1.3 ng/ml X h during the vehicle infusion and 4.1 +/- 1.1 ng/ml X h (P = NS) during the DA infusion. ASF, F, and blood pressure were not altered by upright posture and DA. PAC did not change in the six men infused with DA while supine. Therefore, DA inhibits upright aldosterone responses without affecting PRA, ASF, or F.
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PMID:Dopamine inhibits the aldosterone response to upright posture. 351 47


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