atrial-natriuretic-factor and Hypocapnia

We studied the contributions of hypoxemia, hypocapnia, and hyperpnea to the acute hypoxic diuretic response (HDR) in humans and evaluated the role of peripheral O(2) chemosensitivity and renal hormones in HDR. Thirteen healthy male subjects (age 19-38 yr) were examined after sodium equilibration (intake: 120 mmol/day) during 90 min of normoxia (NO), poikilocapnic hypoxia (PH), and isocapnic hypoxia (IH) (days 1-3, random order, double blind), as well as normoxic voluntary hyperpnea (HP; day 4), matching ventilation during IH. O(2) saturation during PH and IH was kept equal to a mean level measured between 30 and 90 min of breathing 12% O(2) in a pretest. Urine flow during PH and IH (1.81 +/- 0.92 and 1.94 +/- 1.03 ml/min, respectively) but not during HP (1.64 +/- 0.96 ml/min) significantly exceeded that during NO (control, 1.38 +/- 0.71 ml/min). Urine flow increases vs. each test day's baseline were significant with PH, IH, and HP. Differences in glomerular filtration rate, fractional sodium clearance, urodilatin, systemic blood pressure, or leg venous compliance were excluded as factors of HDR. However, slight increases in plasma and urinary endothelin-1 and epinephrine with PH and IH could play a role. In conclusion, the early HDR in humans is mainly due to hypoxia and hypocapnia. It occurs without natriuresis and is unrelated to O(2) chemosensitivity (hypoxic ventilatory response).

Topics: Adult; Atrial Natriuretic Factor; Blood Gas Analysis; Blood Pressure; Carbon Dioxide; Catecholamines; Diuresis; Double-Blind Method; Endothelin-1; Heart Rate; Hormones; Humans; Hyperventilation; Hypocapnia; Hypoxia; Kidney; Kidney Function Tests; Male; Natriuresis; Oxygen; Partial Pressure; Peptide Fragments; Pulmonary Ventilation; Sodium; Time Factors; Urodynamics

To investigate the effects of hypoxemia, hypercapnia, and cardiovascular hormones (norepinephrine, endothelin-1, and atrial natriuretic factor) on blood pressure during acute respiratory failure.. Patients with chronic obstructive pulmonary disease and acute respiratory failure were divided into four groups of 10 patients each: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, and normoxemia-hypercapnia. Plasma norepinephrine levels were determined by high-performance liquid chromatography with electrochemical detection. Plasma endothelin-1 and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction.. Systolic blood pressure and cardiovascular hormone levels were greater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183+/-31 mm Hg and the mean norepinephrine level was 494+/-107 pg/mL, as compared with 150+/- 6 mm Hg and 243+/-58 pg/mL in those with normocapnia and hypoxemia (both P<0.05). Similar results were seen for endothelin-1 and atrial natriuretic factor levels, and for the comparisons of hypoxemic patients who were hypercapnic with those who were normocapnic.. These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respiratory failure, perhaps as a result of enhanced sympatho-adrenergic activity.

Topics: Acute Disease; Adult; Aged; Atrial Natriuretic Factor; Blood Pressure; Carbon Dioxide; Endothelin-1; Female; Heart Rate; Humans; Hypercapnia; Hypertension; Hypocapnia; Hypoxia; Lung Diseases, Obstructive; Male; Middle Aged; Norepinephrine; Oxygen; Respiratory Insufficiency; Severity of Illness Index

1. Hypocapnia has been shown to blunt the natriuretic effect of atrial natriuretic peptide (ANP) independently of the renal nerves. In order to examine whether the adrenal glands are a limiting factor for the natriuretic effect of ANP, we evaluated the natriuretic responses of adrenalectomized rats to ANP infusion during hypocapnia. 2. Rats subjected to total adrenalectomy (ADX) or sham-operation (sham) were divided into hypocapnic and normocapnic groups depending on their arterial PCO2 levels. 3. In sham rats, ANP infusion at a rate of 12 micrograms/kg per h resulted in a smaller increase in the fractional excretion of sodium during hypocapnia (mean +/- SEM: 1.02 +/- 0.40%, n = 10) than normocapnia (3.95 +/- 0.64%, n = 9; P < 0.001). The level of fractional excretion of sodium with ANP infusion during hypocapnia was not significantly different from the level in saline-infused hypocapnic sham rats (0.93 +/- 0.62%, n = 10). In hypocapnic ADX rats (n = 11), ANP induced greater increases in the fractional excretion of sodium (5.59 +/- 1.35%) than did saline infusion (1.04 +/- 1.02%, n = 10; P < 0.002). In the absence of adrenal glands, the magnitude of natriuresis after ANP infusion during hypocapnia and normocapnia (3.32 +/- 1.07%, n = 9) were the same. 4. We conclude that the natriuretic effect of ANP is blunted during hypocapnia in the presence, but not in the absence, of adrenal glands. Our data suggest that the adrenal glands have an important role in limiting the natriuretic effect of ANP.

Topics: Adrenal Glands; Adrenalectomy; Animals; Atrial Natriuretic Factor; Hypocapnia; Male; Natriuresis; Rats; Rats, Wistar

Topics: Atrial Natriuretic Factor; Humans; Hypertension, Pulmonary; Hypocapnia; Hypoxia; Natriuretic Peptide, Brain; Nerve Tissue Proteins

This study evaluated phosphate excretion in response to atrial natriuretic peptide during acute hypocapnia in the presence or absence of the renal nerves in rats. To achieve a hypocapnic state, rats were mechanically hyperventilated with room air. As mechanical ventilation per se has been reported to affect renal excretory functions depending on the ventilatory conditions, this study was designed to examine renal functions during acute hypocapnia as compared with those during normocapnia produced by normal and/or hyperventilation. Rats were divided into three experimental groups: 1) a normally ventilated normocapnic (control) group (n = 8), 2) a hyperventilated normocapnic group (n = 8), and 3) a hyperventilated hypocapnic group (n = 8). The innervated right kidney served as a control for the contralateral denervated kidney. Acute renal denervation produced a greater phosphaturia compared to the innervated kidney during the control period in the two normocanic groups but not in the hypocapnic group. Infusion of ANP 12 micrograms/kg/h produced a remarkable increase in phosphate excretion in either kidney in the normocapnic groups. The degree of the phosphaturia (delta FEPi%) during infusion of ANP was similar between the normally ventilated and hyperventilated normocapnic groups both in innervated (10.6 +/- 2.4% and 7.4 +/- 1.2%) and denervated (14.0 +/- 3.0% and 13.5 +/- 2.2%) kidneys. In contrast to both normocapnic groups, the hypocapnic group had a greater hypophosphaturia during the control and ANP infusion periods in either kidney. The increase in fractional excretion of phosphate was smaller both in innervated (0.34 +/- 0.34% delta FEPi) and denervated (0.72 +/- 0.69% delta FEPi) kidneys than that in the other two normocapnic groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Atrial Natriuretic Factor; Hypocapnia; Kidney; Male; Phosphates; Rats; Rats, Wistar; Sympathetic Nervous System