Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The similar localization of intracranial calcification in hypoparathyroidism and in Fahr disease without parathyroid gland disorder suggests that in these two disorders the pathomechanism of calcium phosphate deposition in the brain may be similar. It may be that in Fahr disease some factors, such as chronic respiratory alkalosis, could lead to hypoparathyroidism-like changes in the brain tissue. Abolition of the phosphaturic response to parathormone (PTH) was recently demonstrated in acute experimental hypocapnia. In three adult patients with Fahr disease, a tendency towards compensatory respiratory alkalosis and arterial hypocapnia was found. The parathormone test revealed a marked decrease in phosphaturia response to PTH, but normal cAMP response. In one patient, the parathormone test was repeated during propranolol administration and showed a considerable improvement in the phosphaturic response to parathormone. It is postulated that chronic hyperventilation and hypocapnia as well as phosphaturic resistance to PTH, intracellular increase of phosphate concentration and development of hypoparathyroidism-like intracranial calcification in patients with Fahr disease could all be caused by disturbance of adrenergic receptors and their relationship to PTH receptors.
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PMID:Abolished phosphaturic response to parathormone in adult patients with Fahr disease and its restoration after propranolol administration. 283 40

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)
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PMID:[Acute hypocapnia attenuates phosphaturic effect of atrial natriuretic peptide in rats]. 775 Jun 24

This study examined the effect of acute hypoxia or hypocapnia on renal phosphate excretion in thyroparathyroidectomized rats. Hypoxia is usually accompanied by a secondary hypocapnia due to hypoxic hyperventilation. Respiratory alkalosis has been described as blunting the phosphaturic effect of parathyroid hormone (PTH). In the present study, to know the effect of hypoxia on renal phosphate excretion in the absence of hypocapnia, the rats were ventilated mechanically, and arterial PCO2 levels were controlled. The rats were divided into three groups depending on the arterial PO2 and PCO2 levels: 1) hypoxic normocapnic group; 2) normoxic normocapnic group; 3) normoxic hypocapnic group. Hypoxia was achieved by ventilating with 10% oxygen, and hypocapnia by hyperventilating with 25-30% oxygen. PTH infusion significantly increased fractional excretion of phosphate (FEPi) from 4.1 +/- 0.9 (mean +/- SE) to 37.7 +/- 2.6% in the hypoxic group (n = 7), from 1.4 +/- 0.3 to 27.4 +/- 2.5% in the normoxic group (n = 8), and from 1.5 +/- 0.4 to 19.5 +/- 1.2% in the hypocapnic group (n = 10). The change of FEPi (delta FEPi) after PTH infusion during hypoxia was significantly greater (33.6 +/- 2.1%) than that during normoxia (26.1 +/- 2.4%, p < 0.05). In contrast to this, hypocapnia blunted the phosphaturic response to PTH (18.0 +/- 1.1% delta FEPi, p < 0.05). Urinary adenosine 3', 5'-cyclic monophosphate (cAMP) increased similarly after PTH infusion in all three groups. To test whether the enhanced phosphaturic effect of PTH during hypoxia and the blunted phosphaturic effect of PTH during hypocapnia are due to steps beyond the production of cAMP, cAMP was administered to the three groups. Cyclic AMP infusion displayed greater phosphaturia in the hypoxic group (n = 6, 30.0 +/- 1.4%) and less phosphaturia in the hypocapnic group (n = 7, 11.3 +/- 1.8%) as compared the the normoxic group (n = 6, 24.1 +/- 1.0%). In conclusion, acute hypoxia enhances the phosphaturic effect of PTH, whereas acute hypocapnia attenuates the phosphaturic effect of PTH.
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PMID:[Phosphaturic effect of PTH during hypoxia and hypocapnia in rats]. 779 27

The objective of this study was to investigate renal phosphate excretion during 24 h of hypoxia in conscious rats fed by total parenteral nutrition. Wistar rats weighing 190 g were exposed to hypoxia (inspired oxygen fraction = 0.10) or normoxia (inspired oxygen fraction = 0.21) for 24 h in a normobaric chamber. Renal clearance and hormonal studies were performed. The results showed a greater fractional excretion of phosphate (5.37 +/- 0.07%, P < 0.05) and hypophosphataemia (7.40 +/- 0.12 mg dL-1, P < 0.01) in hypoxic rats (n = 10) than in normoxic rats (n = 13; 3.50 +/- 0.37% and 8.02 +/- 0.16 mg dL-1, respectively). In addition, during hypoxia there was a significant decrease in the excretion of urinary adenosine 3',5'-cyclic monophosphate per glomerular filtrate (2.97 +/- 1.27 nmol dL-1, P < 0.005), a parameter of the renal action of parathyroid hormone, and a stable level of serum parathyroid hormone (10.2 +/- 2.6 ng mL-1) (cf. normoxia: 8.57 +/- 0.70 nmol dL-1 and 8.0 +/- 1.7 ng mL-1, respectively). However, creatinine clearance and the renal adenosine triphosphate level, both of which affect adenosine 3',5'-cyclic monophosphate excretion, were not different between the two groups. These data suggest that exposure of conscious rats to 24 h of hypoxia causes renal hyporesponsiveness to physiological levels of parathyroid hormone, which is manifested as a decrease in adenosine 3',5'-cyclic monophosphate excretion. Phosphaturia is not a direct net effect of hypoxia and secondary hypocapnia on renal phosphate transport, which is known to be regulated by parathyroid hormone through adenosine 3',5'-cyclic monophosphate.
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PMID:Phosphate excretion during 24 h of hypoxia in conscious rats. 861 26

1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)-treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia. 2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n = 8) or saline vehicle (n = 9). Thirty-minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx- (n = 7) and saline-treated (n = 8) rats. 3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3', 5'-cyclic mono-phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late-phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH-mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline and constant dopamine excretion were observed in endotoxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle. 4. To test whether renal tubular sensitivity to parathyroid hormone related-protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx- (n = 7) and saline-treated rats (n = 7) was examined. Parathyroid hormone related-protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx-than in saline-treated rats. 5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH-mediated phosphaturia after PTH infusion.
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PMID:Renal regulation of phosphate excretion in endotoxaemic rats. 914 87