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Query: UMLS:C0033036 (
APC
)
10,214
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The study was undertaken to clarify the role of atrial natriuretic polypeptide (ANP) in
essential hypertension
(EH). Plasma levels of alpha-human ANP (alpha hANP) were measured in 13 normal subjects, 25 patients with EH, 5 patients with primary aldosteronism (PA), 3 patients with renovascular hypertension (RVH) and 3 patients with pheochromocytoma (PC). Plasma level of alpha hANP (normal: 38.1 +/- 20.5pg/ml) was high in all hypertensive subjects. Synthetic alpha hANP was intravenously administrated to these subjects as follows: first a dose of 0.01 microgram/kg/min for 30 minutes, second a dose of 0.03 microgram/kg/min for 30 minutes, and then in normal subjects and EH 0.03 microgram/kg/min with a dose of 6.5 micrograms/kg/min of metoclopramide (MC) for 30 minutes. After the infusion of 0.01 microgram/kg/min alpha hANP, arterial blood pressure was significantly depressed in EH, RVH and PA, but not in PC. Marked diuretic and natriuretic responses were observed with increase in creatinine clearance and fractional sodium excretion in EH, RVH and PA, but not in PC. Sodium clearance/lithium clearance was slightly increased after infusion of 0.03 microgram/kg/min of alpha hANP in hypertensive subjects. Plasma renin activity did not change in low and normal renin EH and PA after infusion of either dose of alpha hANP, but was suppressed after 0.03 microgram/kg/min of alpha hANP in normal subjects and high renin EH, RVH and PC. Plasma aldosterone concentration was suppressed after either dose of alpha hANP in normal subjects and in EH, RVH and PC, but not in PA. Plasma cGMP concentration and urinary cGMP excretion were decreased after either dose of alpha hANP in both normal and hypertensive subjects. Furthermore, the decrease of
PAC
by alpha hANP was normalized by MC in normal subjects and EH. The rise in plasma cGMP by alpha hANP was suppressed by MC in both normal subjects and EH, but no changes were observed in arterial blood pressure and natriuretic response. These results suggest that alpha hANP secretion increases with elevation of blood pressure in EH, improving increase of circulatory blood volume, and alpha hANP may play a role in elevating blood pressure in EH. Moreover, it is considered that ANP increases sodium and water excretion through its effect on both renal glomeruli and distal tubules in EH. Hypotensive and natriuretic effects of ANP in EH may be concerned with dopaminergic activity which are probably related to the production of cGMP in the vascular wall and inhibition of the excretion of aldosterone in the adrenal cortex.
...
PMID:[The significance of atrial natriuretic polypeptide in the cause of essential hypertension]. 165 13
1. We examined the effects of metoclopramide (MCP: 10 mg i.v.) on plasma atrial natriuretic peptide (ANP) and aldosterone concentrations (
PAC
) and the effect of ANP on MCP-induced
PAC
in four patients with primary glomerular diseases and seven patients with
essential hypertension
. 2. MCP injection caused no significant changes in plasma ANP. MCP produced a marked increase in
PAC
without a significant change in plasma renin activity. 3. The increase in
PAC
induced by MCP injection was markedly attenuated when preceded by the infusion of ANP (25 ng/kg per min). 4. These results suggest that the dopaminergic D2 mechanism is not involved in the regulation of ANP secretion and that ANP modulates the dopaminergic regulation of aldosterone secretion.
...
PMID:Atrial natriuretic peptide inhibits the aldosterone response to metoclopramide in patients with glomerular disease and essential hypertension. 183 3
Clonidine, an agonist of central alpha-2-adrenergic receptors, reduced the peripheral sympathetic activity. With regard to the mutual pathophysiological relationship of blood pressure regulating mechanisms, the authors wanted to find out whether after clonidine administration, in addition to the known suppression of catecholamine levels (CA), also changes in the concentration of other pressor and depressor humoral substances will occur. They investigated therefore in 15 patients with
essential hypertension
(EH) and in three patients with pheochromocytoma the urinary excretion of free noradrenaline (NA), adrenaline (A) and dopamine (DA), the plasma renin activity (PRA), the aldosterone concentration (
PAC
) and atrial natriuretic factor (ANF) in plasma, using radioimmunoanalysis, always before and 24 hours after clonidine administration (Haemiton retardR) by the oral route. Its administration led in patients with EH to a decline of NA and DA. On the other hand, in pheochromocytoma their urinary excretion did not change in an unequivocal way, and when it declined, never normal NA and DA levels were reached. A excretion remained unaltered in both groups of patients. The drop of PRA after clonidine as a result of the drop of peripheral adrenergic activity was not associated with an expected parallel drop of
PAC
but by its rise. This effect can be explained by a reduction of the tonic inhibition of
PAC
output when the DA level declines. The rise of ANF after clonidine administration will be the subject of subsequent investigations. It cannot be ruled out that this effect is due to the direct action of clonidine on alpha receptors in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[The effect of clonidine on humoral factors in patients with arterial hypertension]. 214 Feb 96
The authors investigated dynamic changes and the interaction of the plasma renin activity (PRA), plasma aldosterone (
PAC
), i.e. the main representatives of sodium retaining systems, and of the atrial natriuretic factor (ANF) the decisive natriuretic substance in acute expansion of the extracellular volume (ECV) by infusion of two litres of saline in six controls, seven patients with
essential hypertension
and liver cirrhosis without ascites (6 patients) and with ascites (6 patients). The expansion evoked controversial changes of these systems. It led to a rise of ANF and suppression of
PAC
and PRA. Although ANF rose after infusion to the roughly similar range (12.4 to 15.7 pmol/l), the natriuretic response to expansion differed significantly in different groups of patients. It was most marked in hypertonic subjects (517.2 to 93.2 mumols/min) and practically zero in ascitic liver cirrhosis (54.2 +/- 44.2 mumols/min). The explanation of this finding may be the persistence of high activity of the renin-angiotensin-aldosterone system despite its partial inhibition by infusion of saline in cirrhosis of the liver (PRA 1.69 +/- 0.66 nmols/l/hr.,
PAC
1.12 nmol/l). For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system.
...
PMID:[Mutual interaction of the renin-angiotensin system and the atrial natriuretic factor in the renal response to acute volume loading]. 214 4
The exaggerated natriuretic response to extracellular fluid volume expansion (VE) observed in
essential hypertension
(EH) is related directly to blood pressure (BP) and indirectly to plasma renin activity (PRA). In order to evaluate the precise role of different hormonal parameters, the response to acute VE (isotonic saline, 1,800 ml IV over 3 hours) was assessed in 14 patients with primary aldosteronism (PA, surgically proven adrenal adenoma) and 18 clinically matched EH. At the time of the maneuver, BP and sodium intake were similar in the two groups, but serum potassium (2.89 +/- 0.13 vs 3.69 +/- 0.09 mmol/l), PRA (0.9 +/- 0.2 vs 3.5 +/- 0.9 ng/ml/h) and plasma aldosterone concentration (
PAC
, 25.9 +/- 3.8 vs 12.6 +/- 1.6 ng/dl) were significantly different. During VE, sodium excretion (UNaV) increased more in PA than in EH (98.1 +/- 15.2 vs 63.5 +/- 7.9 mmol/3 h); moreover, the slope of the regression line relating UNAVVE to UNaVcontrol was significantly steeper in PA. By contrast, the change in BP and indices of VE (hematocrit and plasma protein concentration) as well as the decrease in PRA (-45 +/- 9 vs -43 +/- 5 p. 100) and the increase in ANP (+ 65 +/- 16 vs + 69 +/- 28 p. 100) were similar in the two groups. VE left
PAC
unchanged in PA, whilst it decreased
PAC
in EH. We conclude that the natriuretic response to volume expansion is more marked in primary aldosteronism than in
essential hypertension
, a difference which is not explained by variations in the renin-angiotensin system or atrial natriuretic peptide.
...
PMID:[Renal response to acute volume expansion in primary hyperaldosteronism]. 251 Jun 53
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)
...
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.
...
PMID:Changes in haemodynamics and body fluid volume due to enalapril in patients with essential hypertension on chronic diuretic therapy. 302 15
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.
...
PMID:[Effects of high sodium diet on dopaminergic mechanism in normal and hypertensive subjects]. 306 95
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.
...
PMID:Effects of sodium intake on the captopril test for primary aldosteronism. 330 11
To assess the hypothesis that aldosterone may have direct vasoconstrictive action, the acute effects of canrenoate potassium (Soldactone, S), an aldosterone antagonist, on hemodynamics and hormonal responses were determined before and after the intravenous administration of 2 mg/kg S in 11 patients with primary aldosteronism (PA), 9 patients with
essential hypertension
(EH), and 5 patients with renovascular hypertension (RVH). S caused a significant -12 +/- 2 mm Hg decrease in MBP in PA, -5 +/- 2 mm Hg in EH, and -4 +/- 1 mm Hg in RVH. Reduction in MBP was significantly higher in PA than in the others and there was a negative correlation between changes in MBP and basal
PAC
. The cardiac index did not change throughout the study in all groups, which led to a significant reduction in total peripheral resistance index (TPRI) in PA but not in the others. There was a significant correlation between changes in MBP and TPRI (r = 0.82, p less than 0.01). PRA did not change throughout the study, but
PAC
and cortisol were significantly elevated. There were no correlations between changes in MBP and hormonal responses. In conclusion, S resulted in a significant reduction of MBP mediated by a significant reduction of TPRI. These results suggest that aldosterone may have direct vasoconstrictive action and this extrarenal effect of aldosterone may be involved in the regulation of blood pressure.
...
PMID:Extrarenal role of aldosterone in the regulation of blood pressure. 339 Mar 21
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