[Development of natriuretic atrial factor in pregnancy].
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Biomedical subjects
Publications and source records attributed to C Gharib.
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The effects of training alone or in combination with long-term, non-selective, beta-adrenergic blockade on histochemical and biochemical properties of fast-twitch [extensor digitorum longus muscle (EDL)] and slow-twitch [soleus muscle (Sol)] muscle were analyzed in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto strain rats (WKY). Fiber type distribution of Sol was drastically modified in SHR with fewer type I fibers and more type IIA fibers. No such histochemical alterations were observed in EDL. While prolonged swimming training remained ineffective in inducing both histochemical and biochemical improvement in WKY, SHR displayed a significant enhancement of capillarization and oxidative capacity in both Sol and EDL. However, in long-term beta-blocks rats training failed to improve significantly the oxidative capacity of SHR muscles, suggesting that beta-adrenoreceptor stimulation is necessary for a fully efficient adaptation of muscular metabolism to physical training.
To investigate the effects of lower body positive pressure (LBPP) on kidney function while controlling certain cardiovascular and endocrine responses, seven men [35 +/- 2 (SE) yr] underwent 30 min of sitting and then 4.5 h of 70 degrees head-up tilt. An antigravity suit was applied (60 Torr legs, 30 Torr abdomen) during the last 3 h of tilt. A similar noninflation experiment was conducted where the suited subjects were tilted for 3.5 h. To provide adequate urine flow, the subjects were hydrated during the course of both experiments. Immediately after inflation, mean arterial pressure increased by 8 +/- 3 Torr and pulse rate decreased by 16 +/- 3 beats/min. Plasma renin activity and aldosterone were maximally suppressed (P less than 0.05) after 2.5 h of inflation. Plasma vasopressin decreased by 40-50% (P less than 0.05) and plasma sodium and potassium remained unchanged during both experiments. Glomerular filtration rate was not increased significantly by inflation, whereas inflation induced marked increases (P less than 0.05) in effective renal plasma flow (ERPF), urine flow, osmolar and free water clearances, and total and fractional sodium excretion. No such changes occurred during control. Thus, LBPP induces 1) a significant increase in ERPF and 2) significant changes in kidney excretory patterns similar to those observed during water immersion or the early phase of bed rest, situations that also result in central vascular volume expansion.
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We observed a significant increase in plasma atrial natriuretic factor (ANF) in antiorthostatic hypokinetic suspension (AOH) rats after 2 h of suspension when the experiment was made during day. Plasma ANF was investigated in relation to renal glomerular ANF receptors during AOH at night. The aim of this study was 1) to compare the day and night ANF responses to AOH 2) to determine whether the renal glomerular ANF receptors are involved. The rats were divided into 2 groups: i) 24 population cage (PC), and ii) 24 were attached by the tail (Morey's model) and remained in the horizontal position (attached horizontal-AH). Six AH were suspended (30 degrees) for 2 hours (AOH) and sacrificed with the controls: PC and AH (12.00h). The same experiment was made during the night (24.00h). A significant increase in plasma ANF was found in both AOH and AH after 2 h of suspension during day and night (19 +/- 2.3 pg/ml vs 9 +/- 0.95 and 18 +/- 3 pg/ml vs 10.2 +/- 1.8 respectively). PC rats had a significantly higher ANF level (38 +/- 5 pg/ml) than AH or AOH. The glomerular ANF receptor population was slightly lower in AOH than in AH (429 +/- 12 fmol/mg protein vs 507 +/- 5) during day. During night, a significantly lower number of ANF receptors was observed in AOH animals as compared to AH (168 +/- 2 fmol/mg protein vs 455 +/- 3). A decrease in glomerular receptors was also noted in PC during night. Day-time head-down tilt, bed rest or head-out water induced a natriuretic and diuretic response, whereas the normal recumbency at night does not lead to such effects. We conclude that the natriuretic and diuretic response not observed during night was associated with elevated plasma ANF levels and decreased ANF receptor density.
The aim of this study was to determine the effects of a 5-h weightlessness simulation (using supine bed rest or head-down tilt at -10 degrees = HDT) on plasma renin activity (PRA), aldosterone (PA), and catecholamines (epinephrine-E, norepinephrine-NE, and dopamine-DA) and to compare the results with those obtained with horizontal bed rest (BR), which is often taken as a control situation for simulation studies. Ten healthy young volunteers submitted to the three following postural tests: 7 h sitting; 1 h sitting, 5 h supine, and 1 h sitting; 1 h sitting, 5 h HDT, and 1 h sitting. Our results show that a 5-h HDT or BR induced a significant progressive increase in plasma volume (14.5% for HDT and 7% for BR) and a decrease in diastolic blood pressure (18% for HDT and 17% for BR), PRA (60% for HDT and 40% for BR), PA (63% for HDT and 60% for BR), and NE (20% for HDT and 25% for BR) compared to the sitting position. E decreased only in HDT, and DA was unchanged. We concluded that the main part of the cephalad shift is achieved by bed rest as reflected by changes in hematocrit and plasma protein concentration. The decrease in diastolic blood pressure, the inhibition of the renin-angiotensin aldosterone system (in part explained by a decrease in NE) are similar in BR and HDT. We demonstrate that the use of a relevant body position as control is a major concern when investigating the hormonal effects of HDT. If recumbency is chosen as the control situation in HDT studies, it is not surprising to observe only few changes when HDT is applied.
Antiorthostatic hypokinetic suspension (AOH) in rat is currently used as an animal model for simulating weightlessness. This maneuver is responsible for a diuresis, a natriuresis and an increase in central venous pressure (CVP). Knowing the role of CVP in atrial natriuretic factor (ANF) secretion, the aim of the study was to examine the early plasma ANF changes during AOH (angle 30-35 degrees) using Morey's model (tail suspension). The rats were divided into 4 groups: 24 population cage (PC), 24 isolated in separate cages (I), 24 were attached by the tail (Morey's model) and remained in the horizontal position (attached horizontal: AH). At the end of this period of 7 d, 12 AH were suspended for 1, 2, 6 and 24 h (AOH) and sacrificed with the controls for plasma ANF determination. Our results show that the level of ANF is significantly (p less than .05) higher in AOH rats after 2 h of suspension (16.6 +/- 2 pg/ml vs 10.9 +/- 1.5). A significant increase is also observed between AOH and AH after 2h of suspension (p less than 0.05). Six hours after suspension ANF presents a sharp decline in AOH and no difference is observed between AOH and AH and I. Morey's tail suspension model seems to be valid for the study of the early hormonal effects of simulated weightlessness for ANF.
The influence of treadmill or swimming exercise on resting values of plasma and brain arginine vasopressin (AVP), and plasma sodium, potassium, osmolality and proteins was studied after 5 weeks of training using female Wistar rats. The duration of daily training sessions was progressively increased to reach 6 h/day for swim training (S) and 3 h/day for treadmill running (T). Compared to their untrained controls, treadmill and swim training were respectively associated with: a significant lower body weight; a decreased plasma AVP (36.4% for T and 47.4% for S) and hypothalamic AVP (20% for T and 16% for S); a higher hypophyseal AVP (145% for T and 36.3 for S); a decreased plasma osmolality (6.7% for T and 6.1% for S), sodium (1.2% for both) and potassium (15% for T and 22.4% for S); and no change in protein concentration. For T, rectal temperature increased (38.5 +/- 0.20 to 39.7 +/- 0.5) and for S rectal temperature decreased from 38.6 +/- 0.12 to 37.74 +/- 0.10). The differences observed in AVP contents of the pineal and Harderian glands (enhanced only in the treadmill groups) could be explained by the supposed role of these glands in thermoregulation. Two conclusions could be drawn from this study: there are no parallel changes in the hypothalamo-hypophyseal system (where AVP plays its endocrine role) and the brain (where AVP is a neurotransmitter); plasma changes could be explained by an extracellular fluid expansion with Na and K loss leading to a decrease in AVP secretion.
The aim of this work was to study the influence of beta-adrenoreceptor blockade on the adaptation to exercise of one of the hormonal systems (arginine vasopressin) involved in the regulation of blood volume and pressure in spontaneously hypertensive rats (SHR). Systolic blood pressure (SBP) was measured in SHR and WKY rats during 11 wk of swim training. At the end of the training program we determined post-exercise values of plasma arginine-vasopressin (pAVP), osmolality (pOsm), K+ (pK+), Na+ (pNa+), hemoglobin (Hgb), and hematocrit (Hct) in SHR and WKY rats. The following groups were studied: control (C), propranolol treated (PC), swim trained (S), and propranolol-treated and swim-treated (PS). SBP was significantly reduced by swim training or propranolol, bu these beneficial effects on SBP were attenuated when propranolol and swim training were combined. pNa+ and pOsm were significantly reduced by training alone in SHR. This reduction of pNa+ and, consequently, of pOsmol without any modification of other parameters could suggest an Na+ loss. In contrast, the SHR group treated with propranolol alone showed a significant reduction in Hct, suggesting an increased plasma volume without Na+ loss. PS SHR showed a significant reduction of Hgb, Hct, proteins, pNa+, and pOsmol, probably as a consequence of the additive effects of swimming- and propranolol-induced hypervolemia with Na+ loss. The slight and nonsignificant reduction in pAVP observed with either training or propranolol treatment alone became much more pronounced and statistically significant when the 2 treatments were combined. WKY rats showed a much smaller response to exercise and beta-adrenoreceptor blockade than SHR. We conclude that the hypervolemia suggested in PS SHR could be a possible cause of attenuation of the beneficial effects of either swimming or propranolol on SBP.
Plasma levels of ANP were measured during a 4 hrs head-down tilt at -6 degrees in 5 healthy male volunteers (aged 20-22 M.2). The experiments took place from 8 to 14 hrs, (day), and from 22 to 7 hrs (night). The control period was 1 hr. in a seated position (8 to 9 hrs. for day and 22 to 23 hrs. for night). Blood samples were collected at 9 and 23 hrs. and every 20 min. during the first hours, and every hours thereafter. Electroencephalograms were continuously recorded during night. Our results showed a similar increase in ANP during both experimental conditions. During night there was no correlations between ANP and sleep stages. Finally the differences observed in renal responsiveness to central volume expansion during day or night could not be explained by a difference in renin, aldosterone, vasopressin (previously demonstrated in several studies) or ANP secretion.
The effects of propranolol (10 mg/kg) on systolic blood pressure (SBP), resting and exercising heart rates (HR), and body weight (BW) were examined in 11-week swim-trained spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. In both species, SBP was significantly reduced by either propranolol or training, but the reduction was greater with propranolol than with training. However, when propranolol was administered to rats during training, their independent beneficial effects on SBP were annulled. HR was modified slightly by propranolol and training, but they both decreased BW. The mechanism of propranolol action on BW is not clear. Maximum oxygen uptake (VO2 Max), relative heart weight (RHW), and absolute heart weight (AHW) were measured after 11 weeks of training. In both SHR and WKY rats, VO2 Max was elevated by exercise training; moreover, VO2 Max was greatest among those receiving propranolol while training. However, the combined effects of propranolol and training produced a significant reduction of AHW in SHR. The RHW was increased by training, but it was decreased by propranolol. SHR rats were more sensitive to the effects of training and propranolol than WKY rats. In humans, several observations have been reported on the attenuation of certain exercise-induced cardiovascular and metabolic changes by beta-adrenergic blocking agents. Our results obtained with rats confirm some of those observations. It would seem that the hypertensive strain of rats could serve as a model for the study of attenuation mechanisms by beta-adrenergic blockers.
The purpose of this study was to investigate the main renal and hormonal responses to head-down bed rest, which is currently considered a reliable experimental model for the simulation of weightlessness. Urinary output and electrolytes, plasma renin activity (PRA), aldosterone (PA), antidiuretic hormone (ADH) and immunoreactive neurophysin-I (Np) were measured in eight adult volunteers submitted to a 4-day head-down bed rest (-6 degrees) after a 24-h control period in the horizontal position (day 0). Four of the eight subjects were submitted to two 1-h periods of controlled muscular exercise (50% VO2max) from day 1 to day 4. Throughout the head-down bed rest period, urinary output remained stable, although lower than in the control period (day 0), but the urinary Na/K ratio decreased. Plasma electrolytes and osmolality, and creatinine clearance remained unchanged. There was no significant difference between exercising and non-exercising subjects. At the hormonal level, PRA and PA increased during the head-down bed rest. This increase was more pronounced in the group with exercise. At the end of the tilt period, PRA and PA were about 3 times higher than on day 1. No significant changes could be observed for ADH and Np. It is concluded that a 4-day head-down bed rest results in no apparent changes in neurohypophyseal secretory activity, and in a progressive secondary hyperaldosteronism.
Main results of cardiovascular investigation, performed with ultrasound methods during the common French/Soviet flight aboard Salyut VII in June 1982, are compared to variations of the same parameters studied during ground-based simulations on the same subject or observed by other investigators during various ground-based experiences. The antiorthostatic bed rest simulation partly reproduces microgravity conditions and seems to be better adaptated to cardiac hemodynamics, despite some differences, and to the cerebral circulation, than to the inferior limb circulation.
We studied the effects of training by forced swimming on plasma lipid and lipoprotein concentrations in the Lyon genetically hypertensive rats (LH), its normotensive (LN) and low blood pressure (LL) controls. Training was carried out 5 days a week for 5 weeks. The duration of daily training sessions was increased 15 min per day, from 2 to 6 h/day. Following training low density lipoprotein-cholesterol (LDL-C) was significantly lower (P less than 0.01) in LL, and the very low density lipoprotein (VLDL-C) was also lower in LN (P less than 0.01) and LH (P less than 0.05) rats compared with their sedentary controls. High density lipoprotein-cholesterol (HDL-C) was not significantly increased after training in all strains. Compared with controls, plasma total cholesterol, plasma triglycerides and phospholipids were not modified by training. The reduction of LDL-C, VLDL-C as well as the increase of the HDL-C:VLDL-C ratio suggest a beneficial effect of training on atherosclerosis and perhaps coronary heart disease risk.
This study reports the effects of 5 weeks of swim training on systolic blood pressure, body weight, plasma and brain vasopressin and total neurophysins in the Lyon genetically hypertensive (LH) rat and in their normotensive (LN) and low blood pressure (LL) controls. Swimming was unable to influence any studied parameters. These results shed doubt on the efficiency of this model of training on the evolution of hypertension in the LH rats.
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The rate of methionine incorporation was measured in individual hypothalamic nuclei by a quantitative autoradiographic technique: the L-[35S]methionine method. Physiological stimulation of the hypothalamo-neurohypophysial system by two days of water deprivation, a stress that increased the plasma total neurophysins concentration 4-5-fold, resulted in a 70-80% increase in overall protein synthesis in the supraoptic nucleus and in the magnocellular subdivisions of the paraventricular nucleus. The same stimulus had no effect on protein synthesis rate of the suprachiasmatic nucleus and of the other representative cerebral structures examined. This differential effect on protein synthesis was also observed within the paraventricular nucleus.
Head-down bed rest at an angle of 6 degrees was used as an experimental model to simulate the hemodynamic effects of microgravity, i.e., the shift of fluids from the lower to the upper part of the body. The sympathoadrenal activity during acute (from 0.5 to 10 h) and prolonged (4 days) head-down bed rest was assessed in eight healthy men (24 +/- 1 yr) by measuring epinephrine (E), norepinephrine (NE), dopamine (DA), and methoxylated metabolite levels in their plasma and urine. Catecholamine (CA) and methoxyamine levels were essentially unaltered at any time of bed rest. Maximal changes in plasma were on the second day (D2): NE, 547 +/- 84 vs. 384 +/- 55 pg/ml; DA, 192 +/- 32 vs. 141 +/- 16 pg/ml; NS. After 24 h of bed rest, heart rate decreased from 71 +/- 1 to 63 +/- 3/min (P less than 0.01). Daily dynamic leg exercise [50% maximum O2 uptake (VO2 max)] used as a countermeasure did not alter the pattern of plasma CA during bed rest but resulted in a higher urinary NE excretion during postexercise recovery (+45% on D2; P less than 0.05). The data indicate no evident relationship between sympathoadrenal function and stimulation of cardiopulmonary receptors or neuroendocrine changes induced by central hypervolemia during head-down bed rest.