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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether atrial natriuretic factor (ANF) is a circulating hormone in men, a radioimmunoassay suitable for the estimation of ANF in human plasma was developed and the nature of plasma ANF was characterized. Plasma ANF was extracted before radioimmunoassay by affinity chromatography on a column of ANF antibody-coupled agarose. When plasma ANF extract was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, with the radioimmunoassay of the eluted gel slices for ANF, almost all of the ANF activities ran in the 3,000-mol-wt area, while three peaks of ANF were observed in human atrial tissue extract, molecular weights of which corresponded to 14,000, 6,000, and 3,000, respectively. Reversed-phase high performance liquid chromatography of atrial tissue extract resolved multiple forms of ANF. In contrast, one major peak was observed in human plasma extract, and its retention time coincided with that of synthetic human alpha-atrial natriuretic polypeptide. When 500 ml of 0.9% saline was infused into six healthy subjects over 45 min, plasma levels of ANF were unequivocally elevated. The mean plasma ANF concentrations rose from the baseline (23.0 +/- 2.5 pg/ml, mean +/- SEM, n = 6) to the peak (41.8 +/- 4.9 pg/ml, mean +/- SEM) at 75 min postinfusion. No significant change in plasma ANF, on the other hand, was found in the control group. These results suggest that ANF is a circulating hormone in men and is secreted in response to isotonic volume expansion.
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PMID:Atrial natriuretic factor in human blood. 293 72

Atrial natriuretic factor is postulated to act through atrial stretch receptors as a volume regulatory hormone that stimulates diuresis and natriuresis in response to increased atrial pressure. To characterize the stimuli associated with the release of atrial natriuretic factor in humans, we studied 14 normal subjects, both in the supine position and after 10 minutes in an upright posture, while they were on a regular diet (Day 0) and during 3 days of supplemental sodium chloride intake (8 g/day). Radioimmunoassay of plasma atrial natriuretic factor was performed with rabbit antibody to the human hormone amino acids (102-126). Urinary sodium excretion increased from 111 +/- 13 mEq/day (mean +/- SEM) on Day 0 to 275 +/- 15 mEq/day by the third day (Day 3) of high sodium intake. The level of atrial natriuretic factor in the supine position rose from 17 +/- 4 pg/ml (Day 0) to 76 +/- 13 pg/ml on Day 3 (p less than 0.001) and after 10 minutes in an upright posture on Day 3, the level fell to 32 +/- 10 (p less than 0.005). Plasma concentrations of atrial natriuretic factor correlated positively with spot and 24-hour urinary sodium excretion and weight gain, and correlated negatively with plasma aldosterone and renin activity. We conclude that the response of atrial natriuretic factor to sodium loading and posture change in humans is appropriate for a volume regulatory hormone.
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PMID:Sodium loading and posture modulate human atrial natriuretic factor plasma levels. 294 66

Atrial natriuretic peptide is a potent diuretic hormone secreted by the atria in response to volume expansion. We examined the effect of resting tension on atrial natriuretic peptide secretion by rat atria superfused in vitro. Left atria were hooked between an electrode and force transducer and superfused with medium 199. The atria were studied at a pacing frequency of 0 or 3 Hz. Atrial natriuretic peptide content of the superfusate was measured by radioimmunoassay. In nonpaced and paced atria, increasing resting tension three- to five-fold caused immunoreactive atrial natriuretic peptide secretion to increase by 35 +/- 5% (mean +/- SEM, n = 6, p less than 0.01) and 30 +/- 3% (n = 4, p less than 0.01), respectively. Lowering resting tension by 50% in nonpaced and paced atria lowered immunoreactive atrial natriuretic peptide secretion by 30 +/- 3% (n = 7, p less than 0.01) and 24 +/- 3% (n = 6, p less than 0.01), respectively. To exclude the possibility that release of norepinephrine or acetylcholine from endogenous nerve endings was mediating this effect, the atria were superfused with the combination of propranolol 0.1 microM, phentolamine 1.0 microM, and atropine 10 microM. These concentrations of the antagonists were 125-fold or higher than their Kd for binding to their respective receptors. The antagonists did not block the rise in immunoreactive atrial natriuretic peptide secretion; neither did they inhibit an established rise in immunoreactive atrial natriuretic peptide secretion induced by increasing the resting tension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of resting tension on immunoreactive atrial natriuretic peptide secretion by rat atria superfused in vitro. 294 12

Atrial natriuretic peptides (ANPs) circulate in the blood stream and may modulate the regulation of blood pressure, sodium-fluid volume state and renal function. In man, alpha-human ANP (alpha hANP) is probably the major circulating form of ANP. To evaluate its plasma kinetics, we studied in 7 healthy men plasma alpha hANP concentrations under basal conditions and at short intervals during and up to 40 min after discontinuation of a 45-min constant alpha hANP infusion at a rate of 0.1 microgram/min/kg. From basal levels averaging 75 +/- 18 pg/ml (mean +/- SEM), plasma alpha hANP concentrations increased to 1,185 +/- 321 and 1,117 +/- 175 pg/ml at 30 and 40 min during the alpha hANP infusion, respectively. After discontinuing the latter, plasma alpha hANP decreased rapidly, following first-order kinetics, with a plasma half-life of 3.2 +/- 0.4 min. This finding is in line with the brief effects of intravenously applied alpha hANP and suggests that this system may be designed for rapid minute-to-minute adjustments.
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PMID:Plasma kinetics of synthetic alpha-human atrial natriuretic peptide in man. 294 38

In six conscious, trained dogs, maintained on a normal sodium intake of 2 to 4 mEq/kg/day, sympathetic activity was assessed as the release rate of norepinephrine and epinephrine during 15-minute i.v. infusions of human alpha-atrial natriuretic factor. Mean arterial pressure (as a percentage of control +/- SEM) during randomized infusions of 0.03, 0.1, 0.3, or 1.0 microgram/kg/min was 99 +/- 1, 95 +/- 1 (p less than 0.05), 93 +/- 1 (p less than 0.01), or 79 +/- 6% (p less than 0.001), respectively, but no tachycardia and no augmentation of the norepinephrine release rate (up to 0.3 microgram/kg/min) were observed, which is in contrast to comparable hypotension induced by hydralazine or nitroglycerin. The release rate of epinephrine (control, 6.7 +/- 0.6 ng/kg/min) declined immediately during infusions of atrial natriuretic factor to a minimum of 49 +/- 5% of control (p less than 0.001) during 0.1 microgram/kg/min and to 63 +/- 5% (0.1 greater than p greater than 0.05) or 95 +/- 13% (not significant) during 0.3 or 1.0 microgram/kg/min. Steady state arterial plasma concentrations of atrial natriuretic factor were 39 +/- 10 pg/ml (n = 6) during infusions of saline and 284 +/- 24 pg/ml (n = 6) and 1520 +/- 300 pg/ml (n = 9) during 0.03 and 0.1 microgram/kg/min infusions of the factor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of sympathoadrenal activity by atrial natriuretic factor in dogs. 295 27

Studies were performed on anaesthetized Wistar-Kyoto rats to investigate whether the natriuretic response to stimulation of the cerebroventricular system with a hypertonic sodium solution is in part caused by increased plasma concentrations of atrial natriuretic factor (ANF). Through a cannula inserted into a lateral cerebral ventricle a solution with a normal (CSF, 152 mmol l-1) or high (NaCSF, 1,000 mmol l-1) sodium ion content was infused. In the stimulated animals which received NaCSF, the sodium excretion increased more than 13-fold, from 0.07 +/- 0.02 (mean +/- SEM) to 0.97 +/- 0.22 mumol min-1 g-1 kidney wt (P less than 0.01). Potassium excretion rose more than eight-fold, from 0.37 +/- 0.05 to 3.01 +/- 0.13 mumol min-1 g-1 kidney wt (P less than 0.001), and the urine flow rate more than seven-fold, from 1.35 +/- 0.11 to 9.74 +/- 1.23 microliters min-1 g-1 kidney wt (P less than 0.001). The mean arterial blood pressure increased from 100 +/- 3 to 129 +/- 7 mmHg (P less than 0.001). In the control animals which received CSF throughout the experiment there was no significant change in the above variables. The concentrations of ANF in plasma taken at the end of the experiments were determined by a radioimmunoassay. The mean plasma concentration of ANF in animals receiving CSF throughout the experiment was 175 +/- 36 pg ml-1. This was not significantly different from the corresponding value in animals which were given NaCSF (118 +/- 34 pg ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CNS-induced natriuresis is not mediated by the atrial natriuretic factor. 295 71

Plasma atrial natriuretic factor concentrations were measured in 44 patients with mild untreated essential hypertension and 48 normotensive controls. Mean venous plasma atrial natriuretic factor concentrations were 13.2 (SEM 1.5) and 13.0 (1.3) ng/l in the hypertensive patients and controls, respectively. Plasma atrial natriuretic factor concentrations were significantly correlated with age in both groups. Plasma atrial natriuretic factor concentrations were also measured during renal vein catheterisation in a group of 15 hypertensive patients; of these, eight had renovascular hypertension, and in all eight cases plasma atrial natriuretic factor concentrations were increased in the aorta and inferior vena cava. It is concluded that mild essential hypertension is not associated with increased plasma atrial natriuretic factor concentrations, whereas an age related increase in concentrations occurs in hypertensive and normotensive people.
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PMID:Plasma atrial natriuretic factor concentrations in essential and renovascular hypertension. 295 11

Two peptides consisting of amino acids 1-30 and 31-67 of the N-terminal end of the prohormone of atrial natriuretic factor (pro ANF) which vasodilate aortas in vitro, lower blood pressure in vivo, and have natriuretic properties were found to circulate in 54 normal human volunteers. The mean circulating concentration of pro ANF 1-30 was 1861 +/- 87 pg/ml (SEM) while pro ANF 31-67 mean concentration was 1478 +/- 71 pg/ml versus a level of 67 +/- 3 pg/ml for atrial natriuretic factor (ANF). In chronic renal failure their mean concentrations increased to 40,484 +/- 6,929 pg/ml (SEM), 108,566 +/- 16,888 pg/ml, and 348 +/- 81 pg/ml for pro ANFs 1-30 and 31-67 and ANF respectively. Since pro ANF 1-30 and pro ANF 31-67 circulate in man and have physiologic effects they meet the criteria of two new hormones.
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PMID:Two new hormones: prohormone atrial natriuretic peptides 1-30 and 31-67 circulate in man. 296 83

This study was designed to examine the effect of alpha-human atrial natriuretic polypeptide (alpha-hANP) on renin release in the absence of tubules, glomeruli and macula densa. Rabbit afferent arterioles were microdissected and incubated for two consecutive, 20 minute periods. Hourly renin release rate from a single arteriole was calculated. Basal renin release rate was 0.97 +/- 0.13 ng AI.hr-1.Af-1/hr (X +/- SEM, N = 18) and remained stable throughout the incubations. When afferent arterioles were exposed to alpha-hANP (0.01, 0.1 or 1 microM), renin release rate did not change significantly. Isoproterenol (5 microM) increased renin release rate from 0.92 +/- 0.28 to 1.50 +/- 0.46 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). After pretreatment of afferent arterioles with alpha-hANP (1 microM), isoproterenol still increased renin release rate from 0.98 +/- 0.24 to 1.64 +/- 0.37 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). The increases in renin release rate induced by isoproterenol were not different between the two groups. Pretreatment of rabbits with furosemide for two days before experiments resulted in greater basal renin release rates from microdissected afferent arterioles (1.70 +/- 0.35 ng AI.hr-1.Af-1/hr, N = 14). However, exposure to alpha-hANP (1 microM) did not alter this elevated renin release rate. It is concluded that atrial natriuretic factor may not have a direct action on juxtaglomerular cells.
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PMID:Effect of atrial natriuretic factor on renin release in isolated afferent arterioles. 296 64

The relationship between kidney function and plasma immunoreactive atrial natriuretic factor (irANF) levels as well as the effects of synthetic human ANF-(99-126) were investigated in 13 patients with mild to moderate chronic renal failure. Under basal conditions, glomerular filtration rate averaged 39 +/- 5 (SEM) ml/min/1.73 m2 and blood pressure (BP) averaged 166/107 +/- 7/2 mm Hg; 12 patients were hypertensive. Plasma irANF levels were significantly increased (98 +/- 16 vs 42 +/- 4 pg/ml in healthy control subjects; p less than 0.001) and correlated (p less than 0.05-0.005) inversely with hematocrit (r = -0.65) and positively with systolic BP (r = 0.75) or fractional sodium excretion (r = 0.75). Human ANF-(99-126) infusion for 45 minutes at 0.034 microgram/kg/min augmented (p less than 0.05-0.01) diuresis and urinary sodium, chloride, calcium, phosphate, and magnesium excretion. During the subsequent 45 minutes of human ANF-(99-126) infusion at a rate of 0.077 microgram/kg/min, diuresis and electrolyte excretion remained elevated (p less than 0.05-0.01). Glomerular filtration rate and effective renal plasma flow were not significantly modified, but filtration fraction rose progressively (p less than 0.01). Human ANF-(99-126) infusion decreased BP (p less than 0.05-0.01), produced hemoconcentration (hematocrit + 7%; p less than 0.01) without negative body fluid balance, and increased (p less than 0.01-0.001) plasma norepinephrine, insulin, and serum free fatty acids; plasma aldosterone and renin activity were unaltered during but rose after cessation of human ANF-(99-126) infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in mild to moderate chronic renal failure. 296 70


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