Decreased expression of aquaporin 2 in the collecting duct of mice lacking the vasopressin V1a receptor.

BACKGROUND: Vasopressin V1a receptor null (V1aR(-/-)) mice recently showed incomplete urinary concentration due to higher urine volume during control and water diuresis (euhydration), but showed normal response during dehydration (Aoyagi et al., Am J Physiol 295: F100-7, 2008). METHODS: Water balance, plasma vasopressin, plasma and urine osmolality, and aquaporin 2 (AQP2) expression in the kidney of wild-type (WT) and V1aR(-/-) mice were therefore further examined using improved methods of urine collection (urinary bladder urine). RESULTS: V1aR(-/-) mice demonstrated a lower urine osmolality (3,360 ± 138 vs. 3,610 ± 47 mOsm/kgH2O) and a higher plasma osmolality (354.3 ± 1.3 vs. 342.5 ± 1.5 mOsm/kgH2O) after dehydration for 24 h compared to WT mice (P < 0.05). In contrast, the plasma vasopressin concentration was significantly (P < 0.001) higher in the V1aR(-/-) mice (48.8 ± 4.8 vs. 22.1 ± 2.4 pg/ml). On the other hand, although the AQP2 protein expression in the kidney was increased after dehydration, the basal (control) and dehydration-induced AQP2 protein levels were significantly lower in V1aR(-/-) mice compared to WT mice (by Western blotting). Staining by an anti-AQP2 antibody in the luminal membrane of the collecting ducts was increased in both V1aR(-/-) and WT mice after dehydration, but was relatively weaker in the V1aR(-/-) mice (by immunohistochemistry). Moreover, urinary excretion of AQP2 protein, an index of the luminal AQP2 expression, was significantly (P < 0.05) lower in the V1aR(-/-) mice. CONCLUSION: V1aR signaling may be fundamentally important for the expression of AQP2 in the collecting ducts during control conditions and dehydration.

The intercalated cells of the mouse kidney OMCD(is) are the target of the vasopressin V1a receptor axis for urinary acidification.

BACKGROUND: Vasopressin V1a receptor (V1aR) null mice have insufficient acid-base balance, but the target cell for V1aR signaling which results in the urinary acidification has not been identified. METHODS: By using a quantitative in situ hybridization technique and a double-staining technique with an anti-AQP3 antibody in mice, we investigated the axial distribution and acidosis-induced expression of V1aR mRNA along the nephron. We also investigated the acidosis-induced morphological change in the tubule cells from wild-type and V1aR-null (V1aR(-/-)) mice. RESULTS: In the normal condition, V1aR mRNA was moderately expressed in the medullary thick ascending limb (MTAL) and highly expressed in the intercalated cell (IC) throughout the collecting duct (CD). However, no expression was observed in the proximal tubule, thin limbs of Henle's loop, and the principal cell of the CD. Importantly, V1aR mRNA was upregulated significantly both in the TAL and the IC of the CD in the inner stripe of the outer medulla (MTALis and IC of OMCDis, respectively) when mice were treated with NH4Cl (0.28 mol/L) for 6 days. Acidosis-induced hypertrophy, which was completely attenuated in V1aR(-/-) mice, was observed only in the IC of OMCDis (P < 0.005). In addition, urinary excretion of ammonia (NH3/NH4 (+)) was significantly decreased on day 3 (P < 0.05) and day 6 (P < 0.005) in the V1aR(-/-) mice treated with NH4Cl. CONCLUSION: In conclusion, the IC of OMCDis may be the target cell stimulated by the vasopressin V1aR axis and contribute to urinary acidification, at least during metabolic acidosis.

Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney.

BACKGROUND: The calcium (Ca)-activated potassium (K) channel is an alternative K-secretory pathway in the apical membranes of the distal nephrons of adrenalectomized (ADX) animals. As a potential approach for estimating intracellular Ca(2+) increase, we investigated normal and ADX mice to determine whether dietary K intake would stimulate the expression of the calbindin D28k protein, a cytosolic Ca(2+)-binding protein, along the distal nephron consisting of the early and late portions of the distal convoluted tubule (DCT1 and DCT2, respectively), the CNT, and CCD. METHODS: ADX mice received a control diet plus either 0.3% NaCl solution (C) or a 0.3% NaCl plus 3% KCl solution (HK) for 7 days before the experiment. RESULTS: The mean plasma K concentration and pH were significantly (P < 0.001) higher (7.9 ± 0.3 mEq/l) and lower (7.28 ± 0.02) in the K-loaded ADX mice than in the control ADX mice. The mean urinary K excretion (mEq/day) and urine flow (ml/day) increased significantly (P < 0.0001) from 0.47 ± 0.07 (C) to 4.80 ± 0.57 (HK) and from 1.1 ± 0.2 (C) to 8.8 ± 1.0 (HK). Urinary Ca excretion significantly (P < 0.005 and P < 0.05, respectively) increased in K-loaded normal and ADX mice compared with control normal and ADX mice. Immunofluorescence studies revealed that the relative staining of calbindin was 167.0 ± 15.4%, 291.3 ± 13.8%, and 206.3 ± 11.3% for DCT1, DCT2/CNT, and CCD of normal control mice, respectively. These values increased significantly (P < 0.0001) only in DCT2/CNT (574.8 ± 42%) of the K-loaded ADX mice. CONCLUSION: Upregulation of calbindin in the late distal tubule suggests that Ca(2+)-dependent K transport may function as an alternative mechanism for urinary K excretion in ADX mice.

[Two tracheal tubes inserted for endotracheal tube replacement in a patient with severe obstructive sleep apnea: a case report].

A 34-year-old obese, small-jawed and short-necked woman, had severe obstructive sleep apnea syndrome (OSAS) with bronchial asthma. A surgical removal of a lingual tumor using a laser knife was scheduled under general anesthesia with sevoflurane. A small diameter tracheal tube for laser surgery (internal diameter (ID) of 5.5 mm) was used. The tube was inserted using bronchofiberscopy under spontaneous respiration. Extubation was designed to be performed when the patient resumed adequate spontaneous respiration and was awake. However, her ventilation deteriorated postoperatively as spontaneous breathing continued (PaO2 98 mmHg, PaCO2 88 mmHg at FIO2 1.0). This seemed to have been induced by worsened patient-ventilator synchrony and increased airway resistance due to the use of a small diameter tube. We decided to replace the tube with the one with larger diameter. An ID 7.5 mm tube was inserted with the use of fiberscope through the opening of the vocal cord while the tube for laser surgery was left in space. After confirming that the two tubes were inserted securely, the tube for laser surgery was withdrawn. The patient's ventilation improved significantly afterwards and the extubation was performed successfully. Our method for replacing a tracheal tube seemed to be effective and safe.

Anesthetic management of a patient with a history of Batista procedure for dilated cardiomyopathy undergoing gastric surgery.

We experienced anesthetic management for an operation to remove a hemorrhagic gastric submucosal tumor in a patient who had undergone left ventricular volume reduction (the Batista procedure) for dilated cardiomyopathy (DCM) 2 years previously. Preoperative evaluations indicated the relapse of severe DCM. Intravenous and epidural anesthesia was employed with the aid of an intraaortic balloon pump (IABP). Safe anesthetic management was achieved under the guidance of a Swan-Ganz catheter without inducing overreduction of afterload or excessive preload.