Ventricular versus atrial natriuretic factor.
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Animals↗
Biomedical subjects
G Thibault
Publications and source records attributed to G Thibault.
[Physiological analysis of running performance: revision of the hyperbolic model].
1 This paper presents a physiological model for the analysis of the "running curve" (i.e. the relationship between running time and power output) (Table I and Fig. 1). This model is derived from the basic hyperbolic model (Eq. 2: Fig. 2 a) modified in order to take into account the slow adjustment of oxygen utilization and of glycolysis at the onset of exercise (Eq. 7) and the progressive reduction of average aerobic power sustained with increasing running time for races lasting longer than 7 min (Eq. 10; Fig. 2 b, 2 d). 2 This model provides a satisfactory smoothing of the running curve from 200 m to marathon. Average errors (in absolute value) between actual and estimated power output are 0.9 +/- 0.2% (+/- SE) and 1.3 +/- 0.4% for male and female world records respectively (Table II). The basic hyperbolic model (Ptc = A/tc + B) provides a satisfactory smoothing of the running curve on comparatively narrow ranges of events (Table III). 3 Estimations of anaerobic energy stores and of VO2 max made for male and female from world records (1,219 J.kg-1 and 76.4 ml.kg-1.min-1; 1,118 J.kg-1 and 67.8 ml.kg-1.min-1 respectively) are in reasonable agreement with expected values in elite runners (Table IV). 4 The model allows the computation of an objective measure of endurance, i.e. the so-called "ability to sustain a high percentage of VO2 max for a long period of time".(ABSTRACT TRUNCATED AT 250 WORDS)
Energy Metabolism↗
Correlation between ventilatory threshold and endurance capability in marathon runners.
The purpose of the study was to develop an index of endurance capability [i.e., "the ability to sustain a high fractional utilization of maximal oxygen uptake (VO2max) for a prolonged period of time"]. The index was based on the linear reduction of fractional utilization of VO2max with total running time greater than 7 min plotted on a log scale. The endurance index estimated from VO2max, running efficiency and the marathon performance of 18 male runners (30 +/- 7 yr old; VO2max = 66 +/- 5 ml.kg-1.min-1) ranged between -4.07 and -9.96% VO2max.1 nt-1 (mean +/- SD = -6.40 +/- 1.50) and was not related to VO2max (r = 0.107) or speed in the marathon race (r = 0.354). However, the endurance index was closely related (r = 0.853) to the fractional utilization of VO2max at ventilatory threshold (breakaway of the excess CO2 elimination curve) which occurred at 76.1 +/- 5.5% VO2max in response to a graded treadmill test. These results indicate that: (i) running time on long distance races is not, per se, an adequate measure of endurance capability because of the major contribution of VO2max to long distance running performance; (ii) the endurance index expressed as %VO2max.1n t-1 is an objective and independent index of endurance capability; and (iii) runners with a high endurance capability tend to hyperventilate at higher relative workload during a graded treadmill test.
Adult↗
New approaches to predict VO2max and endurance from running performances.
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Adolescent↗
Degradation of atrial natriuretic factor in the rat.
The biologically active circulating form of atrial natriuretic factor (ANF) in the rat is the 28-amino-acid peptide ANF-(Ser-99-Tyr-126). Degradation of this peptide in vivo as well as in vitro, in whole blood, in plasma and by the isolated mesenteric artery was investigated. Studies in vivo in the rat demonstrated that the elimination and degradation of ANF was extremely fast: within 3 min more than 95% of the injected immunoreactive material was eliminated from circulation. The production of a short C-terminal peptide was detected on injection of 125I-ANF-(Ser-99-Tyr-126) into the rat. This peptide increased proportionately with incubation time. Experiments in vitro in the presence of whole blood or plasma did not cause any major destruction of ANF even after incubation for 60 min. After this prolonged incubation in plasma, ANF-(Ser-99-Tyr-126) was partially converted into ANF-(Ser-103-Tyr-126), a less potent peptide. Isolated mesenteric-artery preparation appeared to degrade ANF in a manner very similar to the system in vivo. These results suggest that degradation of ANF may occur either after internalization in the vascular cells or by a membrane-bound enzyme in the vasculature.
Animals↗
The morphine effect on plasma ANF.
The effect of acute morphine treatment on plasma immunoreactive atrial natriuretic factor (IR-ANF) was studied in conscious non-hydrated rats. Morphine treatment induced an 8-fold increase in plasma IR-ANF (P less than 0.001) from 68.1 +/- 9.3 (mean +/- S.E.) to 540.5 +/- 139.5 pg/ml and this increase was completely abolished by pretreatment with the opioid antagonist naloxone (P less than 0.001) to 37.9 +/- 2.8 pg/ml. Naloxone also significantly decreased the basal IR-ANF level (P less than 0.05) to 49.0 +/- 5.3 pg/ml. When naloxone-pretreated and control rats were infused with saline (8 ml) the IR-ANF response was the same in the two groups: 257.7 +/- 64 and 247 +/- 52 pg/ml respectively. Since ANF is a potent natriuretic and diuretic hormone, the morphine-induced increase of plasma IR-ANF may provide a rational basis for explaining the diuretic effect of morphine in conscious non-hydrated rats. Moreover, the decrease of basal plasma IR-ANF suggests the possible implication of endogenous opioids in the regulation of basal ANF secretion.
Animals↗
Atrial natriuretic factor in human plasma.
A reproducible and sensitive radioimmunoassay (RIA) was developed to measure ANF in human plasma. Immunoreactive ANF was extracted from plasma with Sep-Pak cartridges, using 0.2% ammonium acetate (pH 4) with acetonitrile. The sensitivity of the assay was 3.9 pg/ml. The coefficient of variance for inter-assay and intra-assay was 16.8% and 6.8%, respectively. In normal healthy subjects (n = 67), ANF content was 11.9 +/- 1.3 pg/ml (mean +/- SEM). Significantly-higher ANF concentrations were found in proximal coronary sinus blood, being 6 to 37 times greater than in the peripheral circulation. Comparison of the prior extraction method with direct RIA revealed a good correlation (r = 91) in samples containing higher than 100 pg/ml ANF. No correlation was observed with lower values. The elution profiles of reverse-phase HPLC of peripheral and coronary sinus plasma extracts were similar but somewhat complex, with the main immunoreactive peak corresponding to a low-molecular-weight peptide.
Adult↗
Dehydration-induced changes in the secretion of atrial natriuretic factor in Brattleboro rats: effect of water-drinking.
The secretion of atrial natriuretic factor (ANF) was measured in Brattleboro rats (DI) subjected to 20-h dehydration and in normal Long-Evans rats (LE) subjected to 72-h dehydration and 7 times within the hour following voluntary rehydration by drinking water. In these rats, water deprivation caused a large, significant drop in plasma immunoreactive ANF (IR-ANF). Drinking water did not restore plasma IR-ANF values within one hour, even when indirect indices of intravascular volume such as serum osmolality, sodium and hematocrit returned to normal. The dehydration-induced decrease in plasma IR-ANF and its very low secretion after restoring drinking may be essential for the homeostasis of water conservation in both DI and LE rats.
Animals↗
Mechanisms of release of atrial natriuretic factor. II. Effect of chronic administration of alpha- and beta-adrenergic and cholinergic agonists on plasma and atrial ANF in the rat.
The effect that chronic subcutaneous infusion of alpha- and beta-adrenergic and cholinergic agonists on plasma and atrial ANF was investigated. Isoproterenol, a beta-adrenergic agonist, and carbachol, a cholinergic agonist produced a 3-fold increase in plasma ANF levels which were constant until the end of the infusion period. An increased natriuresis was observed in the same groups which was positively correlated with plasma ANF. No differences were observed in atrial content of ANF between the experimental groups. A sharp post-surgery decline in plasma ANF was observed in control, phenylephrine and epinephrine-treated groups which was maintained during the observation period of five days. This suggests that the rise in plasma ANF induced by isoproterenol and carbachol may be secondary to hemodynamic changes and not to direct receptor stimulation, and may play a role in the observed natriuresis. It is also suggested that the depression of plasma ANF may contribute to the well known post-surgery sodium retention.
Adrenergic alpha-Agonists↗
Comparative biological activities of ANF (Arg 101-Tyr 126) and the synthetic form of circulating ANF (Ser 99-Tyr 126).
The biological activities of ANF (Arg 101-Tyr 126) and of the circulating form, ANF (Ser 99-Tyr 126), were compared in the following assays: precontracted rabbit aortic strip and chick rectum, rat natriuresis, inhibition of aldosterone secretion and receptor affinity in bovine and rat adrenal zona glomerulosa cells, and receptor affinity in rabbit aorta and rat mesenteric artery cells. The results demonstrate that both peptides share the same biological activities. It is concluded that the addition of two amino acids to the N-terminal of ANF (Arg 101-Tyr 126) does not modify its biological characteristics, validating thus previous research employing this peptide.
Adrenal Glands↗
Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces.
The effect that several substances may have on ANF release by atrial slices and on its tissular content was investigated. alpha- and beta-adrenergic and cholinergic agonists, vasopressin, met-enkephaline, dexamethasone and DOC, in concentration ranging from 10(-4) to 10(-8) M, were added into the incubation media and incubated 1 and 4 hours. No changes were observed in ANF concentration either in the media or in its tissular concentration as measured by a specific radioimmunoassay. When intact rats were previously treated with DEXA, DOC or DEXA + DOC and their atria incubated "in vitro", an increase in the release of ANF was observed in the Dexa-treated group only, but all treated groups had higher tissular ANF concentration. It is concluded that neither alpha- or beta-adrenergic, nor cholinergic agonists or vasopressin and met-enkephaline stimulate ANF release "in vitro". On the other hand steroids may regulate ANF release and synthesis in the intact rat. It seems likely that the ANF released into the media corresponds to a short peptide.
Animals↗
Receptors for atrial natriuretic factor in cultured vascular smooth muscle cells.
The presence of receptors for atrial natriuretic factor (ANF) was previously demonstrated in the mesenteric vascular bed in rats. Cultured vascular smooth muscle cells obtained from mesenteric arteries of rats were examined for binding of ANF. Saturation and competition experiments demonstrated the presence of a single class of receptors for ANF with high affinity (16 pM) and low capacity. Binding was specific. Kinetic studies showed a dissociation constant which agreed with that obtained at equilibrium in saturation and competition experiments. The exposure of the cells to unlabeled ANF for at least 24 hours showed that ANF may regulate its own receptors in smooth muscle under certain physiological conditions.
Amino Acid Sequence↗
Effect of synthetic atrial natriuretic factor on arginine vasopressin release by the rat hypothalamo-neurohypophysial complex in organ culture.
The effect of synthetic rat atrial natriuretic factor (ANF, Arg 101-Tyr 126) was evaluated in an in-vitro model of rat hypothalamo-neurohypophysial complex (HNC) in organ culture in which part of hypothalamus containing a portion of undamaged magnocellular neurons is separated from posterior pituitary by a fluid tight barrier with an intact stalk connecting both structures. ANF, when added to the medium at the hypothalamus site at concentrations of 3 X 10(-5) M to 3 X 10(-7) M, did not change basal AVP release from the posterior pituitary. Similarly, a shorter form of ANF (Cys 105-Tyr 126), reported to be highly potent in inhibiting adenylate cyclase activity in various tissues, exerted no effect on AVP excretion from HNC in organ culture. The application of an hyperosomotic medium (osmolality 324 +/- 2 mOsm/kg H2O) to the hypothalamic side, together with ANF (3 X 10(-6) M), significantly lowered osmotically-stimulated AVP release. It is concluded that ANF has no effect on basal AVP release from HNC in culture and suppresses osmotically-stimulated AVP secretion in this in vitro model.
Animals↗
Sympathetic response to maximal bicycle exercise before and after leg strength training.
Plasma catecholamine concentrations at rest and in response to maximal exercise on the cycle ergometer (278 +/- 15 watts, 6 min duration) have been measured on seven young active male subjects (19 +/- 1 years old; 80 +/- 3 kg; 176 +/- 3 cm) prior to and after a eight week leg strength training program (5RM, squat and leg press exercise). Strength training resulted in a significant increase in performance on squat (103 +/- 3 to 140 +/- 5 kg) and leg press exercise (180 +/- 9 to 247 +/- 15 kg) associated with a small significant increase in lean body mass (64.5 +/- 2.2 to 66.3 +/- 2.1 kg) and no change in maximal oxygen consumption (47.5 +/- 1.3 to 46.9 +/- 1.2 ml X kg-1 X min-1). Plasma norepinephrine (NE) and epinephrine (E) concentrations (pg X mL-1) were not significantly different before and after training at rest (NE: 172 +/- 19 vs 187 +/- 30; E: 33 +/- 10 vs 76 +/- 16) or in response to maximal exercise (NE: 3976 +/- 660 vs 4163 +/- 1081; E: 1072 +/- 322 vs 1321 +/- 508). Plasma lactate concentrations during recovery were similar before and after training (147 +/- 5 vs 147 +/- 15 mg X dL-1). Under the assumption that the "central command" is reduced for a given absolute workload on the bicycle ergometer following leg strength training, these observations support the hypothesis that the sympathetic response to exercise is under the control of information from muscle chemoreceptors.
Adult↗
Homologous IRCM-serine protease 1 from pituitary, heart atrium and ventricle: a common pro-hormone maturation enzyme?
IRCM-Serine Protease 1 (IRCM-SP1) has recently been isolated and characterized from porcine pituitary anterior and neurointermediate lobes (Cromlish et al., 1986a, J. Biol. Chem. 261:10850-10858; Cromlish et al., 1986b, J. Biol. Chem. 261:10859-10870). This pituitary serine protease was shown to selectively cleave human pro-opiomelanocortin (POMC)-derived peptides at both pairs of basic residues and C-terminal to specific Arg residues, all known to be cleaved in vivo. Here, a similar enzyme was isolated from rat heart atria and ventricles. Rat IRCM-SP1 was shown to be highly specific for the same cleavage sites in POMC, as the porcine pituitary homologue. Furthermore, the rat and the porcine enzymes cleave rat pro-Atrial Natriuretic Factor (pro-ANF 1-126) to yield ANF 103-126, 102-126 and 99-126 in that order of preference. This suggests that in vitro the cleavage sites preferred in pro-ANF resemble those found in brain and hypothalamus. The enzyme is nine times more abundant in atria versus ventricles/mg protein. It is concluded that IRCM-SP1, could well represent a common pro-hormone maturation enzyme for POMC and Pro-ANF and possibly many other pro-hormones.
Adrenocorticotropic Hormone↗
Atrial natriuretic factor and vasopressin during dehydration and rehydration in rats.
To determine the effect of water deprivation (mixed volume and osmotic stimulus) on the secretion of atrial natriuretic factor (ANF) and arginine vasopressin (AVP), plasma immunoreactive ANF (IR-ANF), and plasma AVP were measured in normal conscious Sprague-Dawley rats. IR-ANF was decreased to 19.9 +/- 3.6 pg/ml (24 h dehydration), 9.8 +/- 2.5 pg/ml (48 h dehydration), and undetectable level (72 h dehydration) from the control level of 62.4 +/- 2.4 pg/ml. These decreases were accompanied by significant increase in plasma AVP, serum Na+, osmolality (osm), and hematocrit (Hct). In animals deprived of water for 3 days the secretion of ANF and AVP was monitored at seven time points during the 1st h after voluntary rehydration with tap water. After rehydration, IR-ANF was elevated dramatically within 3 min and gradually for up to 1 h after water was offered; AVP decreased within 3 min of rehydration and stayed at the water-repleted level during the next 1 h. Na+, osm, and Hct did not change until 15, 9, and 30 min after rehydration, respectively. The rapid modifications in plasma IR-ANF and AVP were accompanied by a transient but significant increase in arterial blood pressure for up to 15 min after water consumption. These results indicate that oropharyngeal-gastric stimuli contribute to the release of both ANF and AVP.
Animals↗
Distinct localization of atrial natriuretic factor and angiotensin II binding sites in the glomerulus.
A comparative study of the localization of 125I-labeled atrial natriuretic factor (ANF) and 125I-labeled angiotensin II (ANG II) binding sites in the glomerulus of the rat, after an intravascular injection, has been done by ultrastructural radioautography. 125I-ANF binding sites are localized predominantly on the podocytes of the visceral epithelium (63%) followed by the endothelium of capillaries (14%), the parietal epithelium (13%), and finally mesangial cells (10%). In a comparative study, it was confirmed that 125I-ANG II uptake is localized predominantly on mesangial cells (60%) followed by epithelial visceral cells (23%) and the endothelium of capillaries (16%). Using isolated rat glomeruli, it was confirmed that ANG II decreases glomerular size (maximum effect of 15%) with an apparent half maximum effective concentration (EC50) between 10(-9) and 10(-8) M. Although ANF alone has no apparent effect on glomerular size, it inhibits the contractile effect of ANG II with a half maximum inhibitory concentration (IC50) between 10(-11) and 10(-10) M. These results suggest that an intraglomerular mechanism other than glomerular arteriolar resistance may be involved in the modulation of glomerular filtration rate by ANF. The presence of 125I-ANF uptake mainly in foot processes of visceral epithelial cells of glomeruli in vivo and the inhibition of ANG II decrease in glomerular size by ANF in vitro raise the possibility that ANF may regulate the ultrafiltration coefficient by two mechanisms: modulation of glomerular permeability, and surface area.
Angiotensin II↗
Radioautographic localization of 125I-atrial natriuretic factor binding sites in the brain.
Rats were injected through the carotid artery (cephalad direction) with 18.9 mu Ci of either 125I-Arg 101-Tyr 126 atrial natriuretic factor alone or together with an excess of unlabeled hormone. At 2 min after injection, all rats were fixed in vivo by perfusion and serial sections of the whole brain were processed for light microscope radioautography. The radioautographic reaction produced by 125I-atrial natriuretic factor alone was localized in all circumventricular organs (except the subcommissural organ), the smooth muscle cells and endothelial cells of arteries, arterioles, veins, venules, the endothelial cells of intraparenchymal capillaries and the epithelial cells of the choroid plexus. In rats which received 125I-atrial natriuretic factor plus an excess of unlabeled hormone, the radioautographic reaction was reduced by 70-90%. Binding sites are thus localized in regions of the brain, some of them involved in the central monitoring of blood pressure and osmolarity. In addition, the presence of binding sites in the cerebral vasculature and in the epithelium of the choroid plexus suggests that circulating ANF may play a role in the control of cerebral blood flow and in the production of vertebrospinal fluid.
Animals↗