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)

We reviewed the pathophysiology of our previously reported female patient who had glucocorticoid-responsive hyperaldosteronism and was treated successfully with daily dose of dexamethasone (Dex) for 21 years. In this present study, the possibility that the patient may have 17 alpha-hydroxylase deficiency (17-OH-D) mainly in the adrenal could not be ruled out. We therefore reviewed 31 Japanese patients diagnosed as having 17-OH-D with suppressed plasma renin activity reported in Japan. Among these patients, 9 were found to have a high plasma aldosterone (Ald) concentration (PAC) (group I). Twenty-one patients had either normal or low-normal PAC and the remaining patient had low urine Ald (group II). The slight cross-reactivity of the anti-Ald-antibodies used with 17-deoxy-steroids such as progesterone, 11-deoxycorticosterone and corticosterone which were increased in both groups did not explain the increased PAC in group I. In the patients in group I and group II with high-normal basal PAC, PAC further increased after ACTH and was suppressed by Dex. PAC in 2 group I patients, however, did not respond to angiotensin-II or angiotensin-III infusion. PAC in patients in group II with low or low-normal basal PAC responded equivocally to ACTH and Dex. The basal plasma cortisol in group I was lower than in group II, and plasma cortisol level after ACTH in group I appeared to remain at a lower level than that in group II patients. Among the study subjects, 28 showed a negative correlation between basal PAC and plasma cortisol. A possible discrepancy in the deficiency of 17 alpha-hydroxylase activity in adrenal and gonadal glands was also suggested in three 17-OH-D patients. The pathophysiology of Ald secretion and discrepancy in the deficiency of the enzyme activities in both glands in 17-OH-D patients was discussed.
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PMID:Possible hyperaldosteronism and discrepancy in enzyme activity deficiency in adrenal and gonadal glands in Japanese patients with 17 alpha-hydroxylase deficiency. 255 48

To clarify the role of the sympatho-adrenomedullary and renin-angiotensin-aldosterone systems, and catecholamine receptors, in the pathogenesis of orthostatic hypotension in diabetes mellitus (DM), urinary excretion of catecholamines, and plasma levels of norepinephrine (PNE), epinephrine (PE), renin activity (PRA), aldosterone (PAC), cyclic AMP (PcAMP) and cyclic GMP (PcGMP) were measured in 16 normal subjects (N) and 50 diabetic patients with or without orthostatic hypotension (DMOH(+), DMOH(-)). Changes in PNE, PE, PRA, PAC, PcAMP and PcGMP by standing, glucagon (G) administration and cold pressor test were examined. Furthermore, the effect of metoclopramide on catecholamine levels and blood pressure was investigated before and after cold pressor test. The results were following; (1) Urinary free norepinephrine excretion was significantly lower in DMOH(+), while urinary total norepinephrine excretion was normal in the two DM groups. Urinary free and total epinephrine excretions were lower in DMOH(+) than in N and DMOH(-). (2) PNE and PE were elevated after standing in all groups tested, and more pronounced in some cases of DMOH(+). Although PRA and PAC were elevated normally after standing in all groups, a dissociation between the two parameters was seen in some cases of DM. PcAMP after standing was correlated with PE(r = 0.829). Basal PcGMP was high in many cases of DMOH(+). However, no difference in the elevation of PcGMP after standing was noted between N and the two DM groups. (3) Systolic blood pressure (SBP) rose markedly in only DMOH(+) from 146 +/- 27mmHg to 178 +/- 34mmHg 5 minutes after G administration. The increment of PNE and PE 5 minutes after G administration were similar in all groups. In only DMOH(+), the increase in PcAMP 15 minutes after G test was proportional (r = 0.498) to that of epinephrine. (4) Responses of SBP, PNE, PE and PAC to cold pressor test apparently improved after administration of metoclopramide (MC) in some patients with DM. These results suggest that not only organic disturbance of sympathetic nerves but also functional inhibition of norepinephrine release mediated by dopamine receptor, may play an important role in the pathogenesis of orthostatic hypotension in diabetes mellitus. It is considered that catecholamine secretion from the adrenal medulla in DMOH(+) is increased by hypotension induced by standing. Furthermore, the vascular response to catecholamines may be accelerated through the increment of the extrajunctional receptor in DMOH(+).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The role of the sympatho-adrenomedullary system and adrenergic receptors in the pathogenesis of orthostatic hypotension in diabetes mellitus]. 285 93

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

The present study was designed to clarify the role of serum angiotensin I-converting enzyme (ACE) in the occurrence and maintenance of hypertension in essential hypertension (EH). For this purpose, following experiments were carried out: 1) Correlations between serum ACE activity and renin activity (PRA), aldosterone concentration (PAC) and bradykinin concentration (PBC) in plasma, and blood pressure (BP) as well as serum creatinine levels. 2) Circadian rhythm of serum ACE activity. and 3) Effect of furosemide, upright posture, both furosemide and upright posture, propranolol, indomethacin, 9 alpha-fluorocortisol or angiotensin II (A-II) on the serum ACE activity, PRA, PAC and circulating plasma volume (CPV). The following results were obtained: The serum ACE activity was 30.2 +/- 5.0 U/ml (means +/- SD) in EH as a group, which was significantly higher than that (27.3 +/- 3.9 U/ml) in age matched normotensive subjects (NT) (p less than 0.001). While there was no significant difference in the enzyme activity between low-renin EH (LREH) and NT, a significant difference was found between normal- (NREH) or high-renin EH (NREH) and NT (p less than 0.05 for NREH, p less than 0.01 for HREH). A negative correlation was observed between enzyme activity and age in EH (r = -0.221, 0.05 less than p less than 0.10) as well as in NT (r = -0.306, p less than 0.05). No significant relationships were observed between enzyme activity and BP in either EH or NT. There was a significant positive correlation between enzyme activity and PRA in NT. (r = 0.501, p less than 0.001), NREH (r = 0.658, p less than 0.001) and HREH (r = 0.695, p less than 0.001). However, no significant relationship was found between them in LREH. The enzyme activity was significantly correlated to PAC in NT (r = 0.368, p less than 0.01), NREH (r = 0.567, p less than 0.001) and HREH (r = 0.529, p less than 0.01), but not in LREH. Although no significant correlation was observed between enzyme activity and PBC in NT, NREH and HREH, a significant relationship was found in LREH (r = -0.460, 0.05 less than p less than 0.10). The enzyme activity was not related to serum creatinine levels in EH as well as in NT. In NT, the serum levels of ACE activity reached a maximum values at 6:00 a.m. or 9:00 a.m., and gradually decreased between 6:00 p.m. and 3:00 a.m. An almost similar circadian rhythm of enzyme activity was found in EH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of serum angiotensin I-converting enzyme in essential hypertension]. 300 63

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

Lisinopril (MK521), a lysine analogue of enalaprilic acid, the bioactive metabolite of enalapril, has a longer half-life than enalaprilic acid, and is excreted unchanged in the urine. Its kinetic profile and antihypertensive and hormonal effects have been investigated in an open study in 3 groups each of 6 hypertensive patients, with normal, moderate and severe impairment of renal function. Serum drug level, blood pressure, converting enzyme activity (CEA), plasma renin activity (PRA), aldosterone concentration (PAC), and serum potassium and creatinine were measured during 1 week following a single oral dose and subsequently following 8 daily doses of 5 mg lisinopril. Accumulation of lisinopril was found in the severe renal failure group. CEA was suppressed to less than 10% of its initial value from 4 to 24 h after the initial dose in all three groups, and the suppression was more marked and lasted longer in patients with severe renal failure. An inverse correlation was found in all patients between log serum lisinopril concentration and log CEA. Lisinopril lowered blood pressure in all three groups over 24 h. PRA rose and PAC fell similarly in the groups. Serum potassium increased in the renal failure groups and creatinine remained unchanged in all groups. Thus, when lisinopril 5 mg is given daily to patients with severe renal failure it may accumulate. The high serum lisinopril concentration does not cause an excessive antihypertensive effect. In patients with severe renal failure, adjustment of the dose or the dosing frequency to the degree of renal failure is recommended to avoid administration of doses in excess of those required to achieve adequate inhibition of converting enzyme.
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PMID:Lisinopril in hypertensive patients with and without renal failure. 303 22

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


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