Breathing pattern, CO2 elimination and the absence of exhaled NO in freely diving Weddell seals.

UNLABELLED: Weddell seals undergo lung collapse during dives below 50 m depth. In order to explore the physiological mechanisms contributing to restoring lung volume and gas exchange after surfacing, we studied ventilatory parameters in three Weddell seals between dives from an isolated ice hole on McMurdo Sound, Antarctica. METHODS: Lung volumes and CO(2) elimination were investigated using a pneumotachograph, infrared gas analysis, and nitrogen washout. Thoracic circumference was determined with a strain gauge. Exhaled nitric oxide was measured using chemiluminescence. RESULTS: Breathing of Weddell seals was characterized by an apneustic pattern with end-inspiratory pauses with functional residual capacity at the end of inspiration. Respiratory flow rate and tidal volume peaked within the first 3 min after surfacing. Lung volume reductions before and increases after diving were approximately 20% of the lung volume at rest. Thoracic circumference changed by less than 2% during diving. The excess CO(2) eliminated after dives correlated closely with the duration of the preceding dive. Nitric oxide was not present in the expired gas. CONCLUSION: Our data suggest that most of the changes in lung volume during diving result from compression and decompression of the gas remaining in the respiratory tract. Cranial shifts of the diaphragm and translocation of blood into the thorax rather than a reduction of thoracic circumference appear to compensate for lung collapse. The time to normalise gas exchange after surfacing was mainly determined by the accumulation of CO(2) during the dive. These findings underline the remarkable adaptations of the Weddell seal for restoring lung volume and gas exchange after diving.

Renal and hemodynamic effects of losartan in conscious dogs during controlled mechanical ventilation.

In 12 conscious dogs, we investigated whether the angiotensin II-receptor antagonist losartan increases renal sodium excretion and urine volume during controlled mechanical ventilation (CMV) with positive end-expiratory pressure. In four experimental protocols, the dogs were extracellular volume (ECV) expanded (electrolyte solution, 0.5 ml. kg-1. min-1 iv) or not and received losartan (100 micrograms. kg-1. min-1 iv) or not. They breathed spontaneously during the 1st and 4th hour and received CMV with positive end-expiratory pressure (mean airway pressure 20 cmH2O) during the 2nd and 3rd hours. In the expansion group, dogs with losartan excreted approximately 18% more sodium (69 +/- 7 vs. 38 +/- 5 micromol. min-1. kg-1) and 15% more urine during the 2 h of CMV because of a higher glomerular filtration rate (5.3 +/- 0.3 vs. 4.5 +/- 0.2 ml. min-1. kg-1) and the tubular effects of losartan. In the group without expansion, sodium excretion (2.0 +/- 0.6 vs. 2.6 +/- 1.0 micromol. min-1. kg-1) and glomerular filtration rate (3.8 +/- 0.3 vs. 3.8 +/- 0.4 ml. min-1. kg-1) did not change, and urine volume decreased similarly in both groups during CMV. Plasma vasopressin and aldosterone increased in both groups, and plasma renin activity increased from 4.9 +/- 0.7 to 7.8 +/- 1.3 ng ANG I. ml-1. h-1 during CMV in nonexpanded dogs without losartan. Mean arterial pressure decreased by 10 mmHg in nonexpanded dogs with losartan. In conclusion, losartan increases sodium excretion and urine volume during CMV if the ECV is expanded. If the ECV is not expanded, a decrease in mean arterial blood pressure and/or an increase in aldosterone and vasopressin during CMV attenuates the renal effects of losartan.

Validation and clinical application of a continuous P0.1 measurement using standard respiratory equipment.

The airway occlusion pressure, P0.1, is the negative airway pressure generated during the first 100 msec of an occluded inspiration. P0.1 is a parameter for the neuro-muscular activation of the respiratory system, which is an important determinant for the work of breathing. It has been shown to be a good predictor for successful weaning from mechanical ventilation. Standard P0.1 measurement techniques are based on a total occlusion of the inspiration for more than 100 msec. These measurements are technically complex and therefore not useful for clinical purposes. Furthermore, a significant breath-by-breath variability has been shown for P0.1, which is neglected by any single point measurement technique. Therefore, we have developed a continuous on-line measurement for breath-by-breath determination of P0.1 using the Siemens Servo 900C respirator. In triggered mechanical ventilation the delay time between the onset of the patient's inspiration and flow delivery from the respiratory is more than 100 msec for this respirator. During that time the inspiration is occluded. Therefore, the trigger effort was proposed to be a good estimate of P0.1. Based on this, we calculated P0.1 as follows: airway pressure (Paw) was registered at the endotracheal tube site of the respiratory tubing, digitized and acquired by a personal computer at 100 Hz. The recorder output of the Servo 900C was connected to the same computer, delivering the electronical signal for the inspiratory valve to open when the inspiratory effort has exceeded the trigger threshold, which needs a minimal delay time of 80 msec. Around 20 msec after this signal flow is delivered from the respirator. The computer runs an algorithm, which recognizes this signal and calculates P0.1 (Servo P0.1) as the slope of the pressure drop during this 100 msec. Paw tracings and the calculated P0.1 values were displayed on the computer screen and stored on disk. This method was validated by comparing it to the standard technique, using a Hans-Rudolph valve for inspiratory occlusion and calculating P0.1 from Paw tracings during the occluded inspiration. For validation we used a mechanical lung model which generated P0.1 values ranging between 1.1-10.3 mbar. For a given adjustment of the lung model two standard measurements (standard P0.1) were made and compared to the Servo P0.1. In a total of 21 measurements the mean Servo P0.1 was 4.9 +/- 2.9 mbar; the mean standard P0.1 was 4.3 +/- 2.5 mbar. The mean difference between Servo P0.1 and standard P0.1 was 0.6 +/- 0.6 mbar (range: -0.3-1.8 mbar). The regression equation for linear regression analysis was: Servo P0.1 = 1.15* standard P0.1-0.05. This correlation was significant (r = 0.99, p < 0.01). From these data we conclude that the described method for continuous P0.1 measurement provides reliable values with the advantage of a maneuver-free, breath-by-breath measurement technique. It thereby opens the possibility for monitoring the neuro-muscular activation of the respiratory system at the bedside, which is shown as an example for a patient during weaning from mechanical ventilation.

Influence of captopril on 24-hour balances and the diurnal patterns of urinary output, blood pressure, aldosterone and atrial natriuretic peptide in conscious dogs.

The diurnal time course of urinary flow rate (UV), urinary sodium (UNaV), and potassium (UKV) excretion, and of hormones such as atrial natriuretic peptide (ANP) and aldosterone, was investigated during 5 days of continuous captopril infusion (15 micrograms.kg body weight-1.min-1) in 4 conscious dogs on a high sodium diet (14.5 mmol Na.kg body weight-1.24 h-1). All food and water was given once daily at 8.30 a.m. On the control day and on days 1, 3, and 5 of captopril infusion, urine was collected by an automated system at 20-min intervals over 24 h, blood was taken every 4 h. Mean arterial blood pressure (MABP) and heart rate were evaluated as 5-min averages. Time courses of UNaV, UV, and UKV were compared with the individual control day without captopril. With captopril, 24-hour balances for Na and H2O were slightly negative, while the K balance was slightly positive for 2-3 days. Thereafter, all 24-hour balances were restored. MABP continued to decrease even after Na and water intake and output had come into balance again. Captopril treatment changed the diurnal excretion pattern for UNaV and UV characteristically. In the postprandial period until 5 p.m., less Na and urine were excreted than on the control day, whereas during the evening and night more Na and urine were excreted. The changes in the excretion pattern persisted for the entire observation period. The results indicate that disturbances in the regulating systems, induced by converting-enzyme blockade, bring about complex reactions of, e.g., MABP, ANP and aldosterone that finally restore Na and water 24-hour input/output balances.

Cardiac baroreflex sensitivity and sodium excretion are reduced both by a deficit and an excess of dietary salt in the conscious dog.

In 10 conscious, chronically instrumented beagle dogs we studied the effects of four different dietary sodium intakes (mmol Na/kg body wt/day: 14.5 [excess], 7.5 [high], 2.5 [normal], and 0.5 [low] [plus an additional standardized sodium depletion produced by peritoneal dialysis several days before the experiments]) on cardiac baroreflex sensitivity and renal response to an acute saline load. Full sigmoid barocurves were produced by intravenous injection of phenylephrine (2.5 to 20 micrograms/kg) and nitroglycerine (2.5 to 30 micrograms/kg). The gain of this relationship was significantly decreased by both an excess and low sodium intake (8.0 +/- 1.0 and 8.3 +/- 0.8 beats/min/mm Hg, respectively) when compared with the 2.5 and 7.5 (12.1 +/- 1.4 and 16.0 +/- 1.7 beats/min/mm Hg, respectively) mmol Na/kg/day sodium intake. Water and sodium excretion in response to saline infusion were lower in the 0.5 and 14.5 mmol/kg/day sodium intake groups in spite of the higher atrial natriuretic peptide and lower plasma renin activity and plasma aldosterone levels in the latter. Mean arterial blood pressure, heart rate, and central venous pressure increased during saline loading in all groups; hematocrit and plasma protein concentration decreased similarly in all groups. The results suggest that the rapid renal homeostatic response to an acute salt load in animals kept chronically on normal or moderately increased dietary sodium intake is regulated by baroreflex control of the renal homeostatic response. Excess dietary sodium intake attenuates baroreflex sensitivity and delays sodium and water excretion after acute loading.

ACE inhibition facilitates sodium and water excretion during PEEP in conscious volume-expanded dogs.

Increased activity of the renin-angiotensin system may be involved in sodium and water retention during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP). We therefore evaluated renal, hemodynamic, and hormonal effects of an acute angiotensin-converting enzyme inhibition (ACEI) during PEEP and extracellular volume expansion in five trained chronically tracheotomized dogs. Three protocols were performed: control, 4 h spontaneous breathing with continuous positive mean airway pressure (Paw) of 4 cmH2O (CPAP 4); CMV 20, CPAP for 1st h, CMV with 20 cmH2O Paw for 2 h (2nd and 3rd h), and 1 h of CPAP (4th h); and CMV20-ACEI, ACEI (Ramipril, 2 mg/kg body wt) followed by the same protocol as in CMV 20. During control, sodium excretion (UNaV) and urine volume (V) increased continuously to 56.2 +/- 2.7 (SE) mumol.min-1.kg body wt-1 and 482 +/- 23 microliters.min-1.kg body wt-1, respectively. UNaV and V increased less during PEEP in CMV 20 and CMV 20-ACEI. However, significantly more sodium and water were retained in CMV 20 than in CMV 20-ACEI (2.3 +/- 0.3 vs. 1.0 +/- 0.3 mmol/kg body wt, and 20 +/- 3 vs. 11 +/- 2 ml/kg body wt) because of a decrease of glomerular filtration rate and fractional UNaV in CMV 20. Heart rate did not change in control, CMV 20, or CMV 20-ACEI. Mean arterial pressure increased during control by 13 mmHg, did not change during CMV 20, and was decreased by 7 mmHg in CMV 20-ACEI.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs.

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homeostatic responses to an acute extracellular fluid volume expansion. 2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day-1 kg-1 body weight). 3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min-1 kg-1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 +/- 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments). 4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 +/- 0.3 ml min-1 kg-1 body weight, mean +/- SEM) increased by 1 ml min-1 kg-1. 5. Plasma renin activity [control 0.85 +/- 0.15 (RAP-f) and 1.08 +/- 0.23 (RAP-sc) pmol of angiotensin I h-1 ml-1] decreased similarly in both protocols.(ABSTRACT TRUNCATED AT 250 WORDS)

Computer-assisted long-term measurements of urinary output and other biological data.

A computerized system is described, combining automatic collection of urine in short intervals (minutes) over long periods (days) and recordings of body temperature, MABP, and heart rate in chronically instrumented conscious dogs. During the studies the dogs are housed in metabolic cages. Indwelling catheters and electrical wires are connected to a specially designed swivel and directed out of the cage to the next room. Infusions, blood sampling, and monitoring can be performed from this room without disturbance to the dogs. Three examples of recordings are given. In one of these examples the sodium excretion patterns on 5 consecutive days under continuous saline infusion in one dog is evaluated. Urine was collected every 20 min. Sodium excretion showed cyclic variations. Fourier analysis exhibited 18-h periods and 4- to 8-h periods. The described system renders, e.g., coherent time series analysis possible for a variety of simultaneously recorded physiological variables and may thus acquire considerable importance for integrative physiology.

Acute effects of angiotensin II on renal haemodynamics and excretion in conscious dogs.

The effects of a 60-min intravenous infusion of angiotensin II (A II; 4 or 20 ng A II/min/kg body weight) on renal blood flow (RBF; electromagnetic flow transducer, control value 19-25 ml/min/kg), glomerular filtration rate (GFR; control value 4.2-5.0 ml/min/kg), mean arterial blood pressure, sodium excretion, water excretion, and plasma A II and plasma aldosterone concentrations were examined in 6 chronically instrumented female conscious beagle dogs kept on three different dietary sodium intakes (SI): SI 0.5 or SI 2.5 mmol Na/kg/day or SI 4.5 mmol Na/kg/day plus an oral saline load prior to the experiment SI 4.5(+) dogs. Four nanograms A II decreased RBF and GFR in SI 4.5(+) dogs without changing the filtration fraction (FF%); in SI 0.5 dogs the RBF decreased, and the FF% increased. Twenty nanograms A II decreased RBF and increased FF% in all dietary protocols, less in SI 4.5(+) dogs. The mean arterial blood pressure increased in all dietary protocols by 10-15 mm Hg (4 ng A II) and 32-37 mm Hg (20 ng A II). Sodium and water excretions decreased by 32 and 46%, respectively, in SI 4.5(+) dogs at both doses of A II. The plasma aldosterone concentration increased in all but one protocol: 4 ng A II, SI 4.5(+) dogs. It is concluded that when A II plasma concentrations are most likely borderline to pathophysiological conditions (up to an average of 370 pg/ml), the GFR is less decreased than the RBF. This phenomenon also can be observed at lower plasma A II concentrations (average 200 pg/ml), when the renin-angiotensin system had been previously moderately activated.

Is arterial blood pressure a powerful factor in sodium excretion?

The control of sodium balance is very complex. Many different factors act together in the regulation of renal sodium excretion. Some investigators suggest that arterial blood pressure has a direct effect on urinary excretion of sodium and water. They report that whenever arterial pressure increases, urinary excretion of sodium and water also increases. This phenomenon is called pressure diuresis and natriuresis. It has been stated that an increase in arterial pressure of about 30% can increase urinary output as much as three-fold or more. Many studies, especially in the isolated, perfused kidney, support this idea. However, it is not clear how important this mechanism is under physiological conditions.

Renal sodium handling in intact and renal denervated dogs.

The ability to retain sodium was investigated in six conscious dogs before and after surgical renal denervation. Dietary sodium and water intake were kept constant (2.5 mmol Na X kg-1 bw X day-1 and 91 ml water X kg-1 bw X day-1). Balance experiments were performed from 6 days before to 8 days after having produced a sodium deficit of 6.4 +/- 0.4 (intact dogs) and 5.8 +/- 0.2 (renal denervated dogs) mmol Na X kg-1 bw by means of a peritoneal dialysis (PD). Having the same sodium excretion before PD, intact and renal denervated dogs demonstrated a similar striking decrease of sodium excretion and a similar increase of plasma renin activity after PD until the amount of sodium lost had been replenished (4th day after PD). In intact and renal denervated dogs plasma sodium concentration (PNa) decreased and renal water excretion increased on the first day after PD, indicating a homeostatic response to the fall of PNa. After dietary sodium restriction (from 2.5 to 0.5 mmol Na X kg-1 bw X day-1) a similar striking decrease of renal sodium excretion occurred in intact and renal denervated dogs. It therefore is concluded that in conscious dogs the presence of the renal nerves is not essential in order to maintain body sodium homeostasis after an acute sodium loss or after dietary sodium restriction.

Acute effects of angiotensin II in intact and adrenalectomized conscious dogs.

UNLABELLED: Renal effects of A II, retention of sodium and water, may be mediated by the stimulation of aldosterone secretion and/or by direct effects of A II on the kidneys. An attempt was made to differentiate between these two possibilities. METHODS: Conscious, female beagle dogs were used. The dogs were kept under standardized conditions (metabolic cage, daily sodium intake 4.5 mmol X kg-1 bw, chronically implanted arterial and venous catheters, i.v. hormone substitution after adrenalectomy by a portable pump). A II was infused i.v. over a period of 60 min after 60 min control. (Rate: 1, 4, 20 or 200 ng X min-1 X kg-1 bw). RESULTS: Mean arterial blood pressure (MABP) increased with 20 and 200 ng A II X min-1 X kg-1 bw by an average of 34 mm Hg and 65 mm Hg resp. before and after adrenalectomy. Before adrenalectomy: sodium and water excretion decreased always at 4 and 20 ng A II X min-1 X kg-1 bw, whereas a rate of 200 ng A II X min-1 X kg-1 bw had different effects on renal sodium and water excretion. After adrenalectomy: sodium and water excretion decreased at 4 ng A II X min-1 X kg-1 bw. Whereas a rate of 20 and 200 ng. -As no marked alterations of the glomerular filtration rate occurred, sodium retention observed was mainly due to tubular effects of A II. Plasma aldosterone concentration increased at 4, 20 and 200 ng A II X min-1 X kg-1 bw in the intact dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

An attempt to quantitate the contribution of antidiuretic hormone to the diuresis of left atrial distension in conscious dogs.

In order to quantitate the contribution of the antidiuretic hormone (ADH) to the diuresis of left atrial distension 52 experiments have been performed in 12 conscious, chronically instrumented beagle dogs. Left atrial pressure was increased by a reversible mitral stenosis by about 10 cm H2O (1.0 kPa) for 60 min. Plasma ADH concentration (range between 1.3 and 6.0 pg . ml-1) (radioimmunoassay) decreased in every experiment, the average decrease being about 50%. An i.v. infusion of vasopressin (0.05 mU . min-1 . kg-1) abolished the diuretic effect of left atrial distension or decreased the urine volume below control values; natriuresis was not affected. The magnitude of the vasopressin effect was dependent on the concurrent sodium excretion: when sodium excretion was low during left atrial distension, vasopressin was more effective in reducing the urine volume than when sodium excretion was high. It is concluded that the diuresis of left atrial distension is mediated (a) by a suppression of ADH and (b) by factors controlling sodium excretion, the contribution of these two mechanisms being dependent on the concurrent sodium excretion.

Estimation of glomerular filtration rate in conscious dogs following a bolus of creatinine. Comparison with simultaneously determined inulin clearance.

The renal clearance of creatinine was measured following orogastric administration in conscious dogs. Values of creatinine clearance were compared with simultaneously determined values of inulin clearance, when urine volume, glomerular filtration rate and volume status were acutely altered by a variety of experimental manoeuvres. At urine volumes greater than 20 microliters X min-1 X kg-1, creatinine clearance was not significantly different from inulin clearance. At low urine volumes there was some evidence of creatinine reabsorption. It is concluded that the bolus creatinine technique provides reliable estimates of glomerular filtration rate and is particularly applicable to long-term studies in conscious dogs.

The control of sodium metabolism to maintain osmo- and volumehomeostasis.

Chronically instrumented female beagles were maintained in standardized environmental and dietary conditions allowing careful examination of the mechanisms governing sodium homeostasis. The experimental increase in left atrial pressure (obtained by a reversible mitral stenosis) is accompanied by an increase in sodium excretion (atrial natriuresis, AN). AN served as an experimental manoeuvre from which the mechanisms governing sodium homeostasis could be elucidated. The results allow the following conclusions: (1) The 'signals' arising from distension of the left atrium (e.g. expansion of the extracellular fluid volume) appear not to be a necessary prerequisite for the maintenance of sodium homeostasis. (2) The control mechanisms seem to be very sensitive to changes in total body sodium (TBS). A small reduction in TBS abolishes sodium eliminating processes e.g. saline diuresis, osmotic diuresis, AN. (3) It is probable that a natriuretic factor exists for sodium elimination. In summary, total body sodium appears to be controlled by a series of 'redundant' mechanisms which guarantee an appropriate strategy for the comfort and ultimate survival of the organism. At the moment it is impossible to quantitate the contributions made by the various mechanisms in the control of sodium metabolism.

The role of the cardiac nerves in regulation of sodium excretion in conscious dogs.

Conscious, chronically instrumented dogs, maintained on a high sodium intake, were used to investigate whether surgical cardiac denervation impairs the natriuresis associated with left atrial pressure increase produced in three ways: during an increase in left atrial pressure by means of a reversible mitral stenosis (protocol 1); after an i.v. saline load (1.0 ml 0.9% saline min-1 . kg-1 over 60 min) (protocol 2); after an oral saline load (14.5 mmol Na . kg-1 given with the food as isotonic solution) (protocol 3). During a reversible mitral stenosis, in intact dogs, urine volume and sodium excretion increased markedly (from 34--145 microliters . min-1 . kg-1 and from 3--12 mumol . min-1 . kg-1); mean arterial pressure increased by an average of 2 kPa (15 mm Hg) and heart rate by 53 b/min; plasma renin activity fell from 0.37--0.21 ng AI . ml-1 . h-1 . Cardiac denervation eliminated these effects of left atrial distension except for a small increase in heart rate (12 b/min). This indicates that the natriuresis and diuresis during left atrial distension resulted from stimulation of receptors located in the left atrium. In contrast, during protocol 2 and 3, the same amounts of sodium and water were excreted in the cardiac denervated dogs as compared to the intact dogs. A comparable decrease in plasma renin activity also was observed. -- Apparently the presence of the cardiac nerves is not a prerequisite for maintenance of sodium and water homeostasis.

Left atrial distension and intrarenal blood flow distribution in conscious dogs.

Measurements were made with radioactive microspheres of the distribution of renal blood flow in conscious dogs during left atrial distension. Urine volume, sodium excretion, mean arterial blood pressure and heart rate increased during the 60 min period of left atrial distension (increase in left atrial pressure by about 1.0 kPa). Total renal blood flow and cardiac output (electromagnetic flowmeters) did not change. The perfusion rates of four renal zones did not change. Striated muscle blood flow (M. psoas) fell markedly.--Stimulation of left atrial receptors in conscious dogs is followed by an increase in renal and skeletal muscle resistance. The diuresis and natriuresis during left atrial distension is not accompanied by a detectable redistribution of renal cortical blood flow.

Atrial natriuresis under the condition of a constant renal perfusion pressure: experiments on conscious dogs.

An experimental elevation of left atrial pressure (eLAP) by means of a reversible mitral stenosis is accompanied with an increase in sodium excretion (UNaV) and arterial blood pressure (by about 20 mm Hg, 2.7 kPa), and by a decrease in plasma renin activity. It is well established that an increase in renal perfusion pressure (Pren) can augment UNaV. Therefore the present study was undertaken to examine whether the eLAP-induced natriuresis was caused by the increased Pren. -Four female beagle dogs were kept under controlled environmental conditions. They received a sodium rich diet (14.5 mmol/Na/kg/d). The dogs were chronically instrumented: purse string around the mitral annulus, catheter in the left atrium, carotid loop, pneumatic cuff above the renal arteries, pressure transducer below the renal arteries. Pren was kept constant by means of a digital servofeedback control circuit. The dogs served as their own controls (13 experiments without and 15 experiments with a controlled renal perfusion pressure were performed). After eLAP(+1.0 kPa), UNaV rose from 4.1 +/- 2.6 to 10.3 +/- 3.9 mumol Na/min/kg. If Pren was kept constant, the corresponding values were 4.2 +/- 2.8 and 9.3 +/- 2.9 mumol/min/kg. These data clearly indicate that the atrial natriuresis is not mediated by an augmentation of renal perfusion pressure. Therefore these results support the hypothesis that atrial natriuresis probably is due to en eLAP-induced suppression of the renin-angiotensin-system or other natriuretic mechanisms.