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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of hypobaric hypoxemia on endocrine and renal parameters of body fluid homeostasis were investigated in eight normal men during a sojourn of 8 days at an altitude of 4,559 m. Endocrine and renal responses to an osmotic stimulus (5% hypertonic saline, 3.6 ml/kg over 1 h) were investigated at sea level and on day 6 at altitude. Several days of hypobaric hypoxemia reduced body weight (-2.1 +/- 0.4 kg), increased plasma osmolality (+5.3 +/- 1.4 mosmol/kgH(2)O), elevated blood pressure (+12 +/- 1 mmHg), reduced creatinine clearance (122 +/- 6 to 96 +/- 10 ml/min), inhibited the renin system (19.5 +/- 2.0 to 10.9 +/- 0.9 mU/l) and plasma vasopressin (1.14 +/- 0.16 to 0.38 +/- 0.06 pg/ml), and doubled circulating levels of norepinephrine (103 +/- 16 to 191 +/- 35 pg/ml) and endothelin-1 (3.0 +/- 0.2 to 6.3 +/- 0.6 pg/ml), whereas urodilatin excretion rate decreased from day 2 (all changes P < 0.05 compared with sea level). Plasma arginine vasopressin response and the antidiuretic response to hypertonic saline loading were unchanged, but the natriuretic response was attenuated. In conclusion, chronic hypobaric hypoxemia 1) elevates the set point of plasma osmolality-to-plasma vasopressin relationship, possibly because of concurrent hypertension, thereby causing hypovolemia and hyperosmolality, and 2) blunts the natriuretic response to hypertonic volume expansion, possibly because of elevated circulating levels of norepinephrine and endothelin, reduced urodilatin synthesis, or attenuated inhibition of the renin system.
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PMID:Prolonged hypobaric hypoxemia attenuates vasopressin secretion and renal response to osmostimulation in men. 1196 Sep 41

Mannitol overuse-induced acute renal failure (ARF) has rarely been described. We report four cases, all male, between the ages of 20 and 42 years, who developed acute renal failure (3 anuric, 1 nonoliguric) after receiving mannitol 1,172 +/- 439 g (mean +/- SD) during a time period of 58 +/- 28 h. The infusion rate was 0.25 +/- 0.02 g/kg/h. The onset of acute renal failure was detected 48 +/- 22 h after infusion. In 2 of the 3 cases in which urinary cytology was evaluated, the presence of vacuole-containing renal tubular cells was observed. All patients had hyponatremia (120 +/- 11 mEq/l), and hyperosmolality (osmolar gap 70 +/- 11 mosm/kg water). No other factors could be pointed to as causing acute renal failure. In the 3 anuric cases in which hemodialysis was performed, immediate recovery of diuresis was observed. Two patients recovered renal function on the fifth and sixth days, and 2 died due to endocranial hypertension - one of them while recovering - on the fourth and sixth days. In the present report, mannitol-induced ARF occurred at clustered doses of 0.25 mg/kg/h.
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PMID:Acute renal failure following massive mannitol infusion. 1238 62

The reference method to measure serum osmolality (Mosm) is the delta cryoscopic method. However, the technology may not be available. Clinicians therefore must calculate osmolality (Cosm) as the sum of concentrations of selected principal solutes such as sodium, potassium, urea, and glucose. To evaluate the validity of Cosm in patients in hyperosmolar state we compared Cosm to Mosm. Twenty-two ICU patients treated by infusion of hypertonic solutes for intracranial hypertension following head injury were prospectively studied. A control group of 10 patients with hypernatremia due to medical causes was also evaluated. Na+, blood urea nitrogen (BUN), and glucose were measured to calculate serum osmolality: Cosm = (2 x Na+) + BUN + glucose (in mOsm/kg). Measurement of serum osmolality was performed using the delta-cryoscopic method. The results of the two methods were compared by correlating the difference (Mosm-Cosm) between each pair of results with the mean of the pairs of results. Cosm underestimated Mosm (3.4 mOsm/kg, P < 0.02) in the control group whereas Cosm overestimated Mosm in patients who received hypertonic fluids (2.3 mOsm/kg, P < 0.03). Calculation of osmolality introduced a systematic bias, overestimating osmolality in the lower ranges and underestimating it in the higher ranges. In the range of hyperosmolality commonly used to manage intracranial hypertension following head trauma, serum osmolality, as determined by sum of principal serum solutes, compares poorly with direct measurement using standard osmometry.
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PMID:Calculated serum osmolality can lead to a systematic bias compared to direct measurement. 1584 Sep 98

1. Accumulating evidence in both humans and animals indicates that acute increases in plasma osmolality elevate sympathetic nerve activity (SNA). In addition, plasma hyperosmolality (or hypernatraemia) can produce sustained increases in SNA and arterial blood pressure (ABP) through stimulation of forebrain osmoreceptors. 2. Although an abundance of information exists regarding the osmoregulatory circuits for thirst and secretion of antidiuretic hormone, much less is known about those pathways and synaptic mechanisms linking osmotic perturbations and SNA. To date, the available evidence suggests that osmosensitive sites within the forebrain lamina terminalis, such as the organum vasculosum of the lamina terminalis, are key elements that link plasma hypertonicity to elevated SNA. 3. The major efferent target of osmosensitive regions in the forebrain lamina terminalis is the hypothalamic paraventricular nucleus (PVH). Evidence from a number of studies indicates that the PVH contributes to both acute and chronic osmotically driven increases in SNA. In turn, PVH neurons increase SNA through a direct vasopressinergic spinal pathway and/or a glutamatergic pathway to bulbospinal sympathetic neurons of the rostral ventrolateral medulla. 4. Future studies are needed to: (i) define the contribution of various osmosensitive regions of the forebrain lamina terminalis to acute and chronic osmotically driven increases in SNA; (ii) identify the cellular mechanisms and neural circuitry linking plasma osmolality and SNA; and (iii) define whether such mechanisms contribute to elevated SNA in salt-sensitive hypertension.
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PMID:Forebrain osmotic regulation of the sympathetic nervous system. 1806 92

It is well known that cardiovascular alterations are the principal causes of mortality in patients with diabetes. Premature and accelerated atherosclerosis cannot be the sole cause of diabetic heart disease because functional disorders develop both in experimental and in clinical diabetes before the onset of the detectable morphological changes of the vessel wall. Namely, altered adrenergic responses and prostaglandin metabolism and diminished vasodilatory ability can be seen in diabetic vessels. This leads to enhanced vasoconstriction, which - combined with increased sympathetic activity - may induce myocardial edema and an increase in myocardial stiffness, resulting in diminished heart function. Increased myocardial stiffness due to myocardial dehydration caused by hyperglycemic hyperosmolality can also result in impaired heart function. Thus, myocardial water content plays a key role in the development of diabetic heart dysfunction. Disturbances in the myocardial energy metabolism may also contribute to the diminished cardiac performance in the diabetic state. Some antidiabetic agents may also have deleterious cardiovascular effects. Whether the functional abnormalities observed in the reviewed studies lead to clinically manifest heart disease in diabetes may depend on the superimposition of the classical cardiovascular risk factors. Thus, adequate control of carbohydrate and lipid metabolism and the possible concomitant hypertension may prevent the further impairment of heart function and the development of overt heart disease.
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PMID:The diabetic heart: A review of the lifework of Sophie Maria Koltai. 1964 94

Demyelination is characterized by the loss of myelin with the preservation of axons. Demyelinating diseases can be classified into several categories: demyelination due to inflammation, viral infection, osmotic derangements and hypoxic ischemia. In particular, osmotic myelinolysis is representative, and is associated with hyperosmolality, hypokalemia or rapid correction of hyponatremia. Osmotic myelinolysis was reported to be associated with underlying conditions, such as alcoholism, diuretics and malnutrition. A 67-year-old woman with hypertension was scheduled to undergo both total knee replacements (TKR). She was observed to be lethargic with dysphagia and quadriplegia after the second TKR. She had been taking diuretics for a long time, and did not have an adequate amount of food intake due to patient controlled analgesia and a gastric ulcer after the first TKR. A laboratory examination revealed hypokalemia but normonatremia. T2 weighted-MRI revealed abnormal high signal intensity in the basal ganglia and periventricular area. This case was diagnosed with osmotic myelinolysis associated with hypokalemia without an apparent sodium imbalance.
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PMID:Extensive demyelinating change in cerebrum after a total knee replacement -A case report-. 2128 40

An 11-year-old spayed female domestic shorthair cat was evaluated for anorexia, lethargy and weight loss of 6 days' duration. Bilateral mydriasis, absent menace response, slow-to-absent pupillary light reflexes, bilateral retinal detachment, intermittent horizontal nystagmus, intermittent ventral strabismus and systemic hypertension were present. Biochemical analysis revealed severe hyponatremia, severe hypochloremia and mild hypokalemia. Multifocal central nervous system disease was suspected based on optic, trigeminal sensory (ophthalmic branch), vestibulocochlear and possible oculomotor nerve dysfunction. Thoracic radiographs showed mild cardiomegaly without evidence of congestive heart failure. Ultrasound revealed mild pleural and peritoneal effusion. A cause of the severe hyponatremia was not identified, and it persisted despite fluid therapy. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) was suspected as the cause of hyponatremia. Humane euthanasia was elected owing to continued clinical decline. Serum hyposmolality, urine hyperosmolality, natriuresis and lack of confirmed renal, thyroid and pulmonary disease aided in the presumed diagnosis of SIADH. Post-mortem histopathology of the brain revealed degeneration of the hypothalamus and optic tracts, along with a prominent fluid-filled craniopharyngeal duct (putative Rathke's cleft cyst) separating the pars distalis and the pars intermedius. The hypothalamic degeneration, possibly secondary to a Rathke's cleft cyst, was hypothesized to be the cause of presumptive SIADH in the patient. Although rare in occurrence, Rathke's cleft cyst should be included as a differential diagnosis in dogs and cats with signs of pituitary dysfunction.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in a cat with a putative Rathke's cleft cyst. 2465 77

Neonatal renal vein thrombosis (RVT) is associated with potentially serious morbidities. Almost 80% of cases of RVT present within the first postnatal month. The most common risk factors for RVT are birth asphyxia/ in utero fetal distress, being the infant of a diabetic mother, volume contraction and coagulation abnormalities. Thrombus formation may be initiated by vascular injury, diminished vascular flow, increased blood viscosity, hyperosmolality or underlying thrombophilia. The classic triad of RVT includes gross hematuria, flank mass (unilateral or bilateral enlargement of kidneys) and thrombocytopenia. Laboratory tests may reveal hematuria, proteinuria, polycythemia, hemolytic anemia, thrombocytopenia and possibly acute kidney injury. The etiology for a hypercoagulable state should be investigated. Renal ultrasound with Doppler may show increased size of the affected kidney, increased echogenicity and loss of corticomedullary differentiation. Renal venography remains the gold standard for the diagnosis of RVT. Other causes of renal enlargement must be considered. Supportive treatment includes correction of fluid and electrolyte disturbances and treatment of infection and underlying pathophysiologic abnormalities. Use of unfractionated heparin (UFH) or low molecular weight heparin (LMWH) should be considered if there is evidence of disseminated intravascular coagulation. Conventional anticoagulants may attenuate hypercoagulability and decrease the risk for thrombus progression and embolism. Surgery is rarely indicated unless there is bilateral involvement with involvement of the IVC. RVT carries the risk of hypertension and chronic kidney disease.
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PMID:Renal venous thrombosis in neonates. 2508 63

The common notion is that the body Na+ is maintained within narrow limits for fluid and blood pressure homeostasis. Several studies have, however, shown that considerable amounts of Na+ can be retained or removed from the body without commensurate water loss and that the skin can serve as a major salt reservoir. Our own data from rats have suggested that the skin is hypertonic compared with plasma on salt storage and that this also applies to skin interstitial fluid. Even small electrolyte gradients between plasma and interstitial fluid would represent strong edema-generating forces. Because the water accumulation has been shown to be modest, we decided to reexamine with alternative methods in rats whether interstitial fluid is hypertonic during salt accumulation induced by high-salt diet (8% NaCl and 1% saline to drink) or deoxycorticosterone pellet implantation. These treatments resulted both in increased systemic blood pressure, skin salt, and water accumulation and in skin hyperosmolality. Interstitial fluid isolated from implanted wicks and lymph draining the skin was, however, isosmotic, and Na+ concentration in fluid isolated by centrifugation and in lymph was not different from plasma. Interestingly, by eluting layers of the skin, we could show that there was an osmolality and urea gradient from epidermis to dermis. Collectively, our data suggest that fluid leaving the skin as lymph is isosmotic to plasma but also that the skin can differentially control its own electrolyte microenvironment by creating local gradients that may be functionally important.
Hypertension 2017 04
PMID:High-Salt Diet Causes Osmotic Gradients and Hyperosmolality in Skin Without Affecting Interstitial Fluid and Lymph. 2816 86

The distal tubule and collecting duct in kidney regulate water homeostasis. TMOD1 is an actin capping protein that plays an important role in controlling the organization of actin filaments. In this study, we found TMOD1 was specifically expressed in distal tubules and collecting ducts. To investigate the role of TMOD1, we created Tmod1flox/flox mice and bred them with Ksp-Cre mice to generate tubule-specific Tmod1 knockout mice, Tmod1flox/flox/Ksp-Cre+ (designated as TFK). As compared with control mice, TFK mice showed oliguria, hyperosmolality urine, and high blood pressure. To determine the mechanisms underlying this phenotype, we performed label-free quantitative proteomics on kidneys of TFK and control mice. Total of 83 proteins were found differentially expressed. Bioinformatic analysis indicated that biological processes, including protein phosphorylation and metabolic process, were involved in TMOD1 regulatory network. Gene set enrichment analysis showed that multiple pathways, such as phosphatidylinositol signaling system and GnRH signaling pathway, were strongly associated with Tmod1 knockout. Western blot validated the down-regulation of three proteins, TGFBR2, SLC25A11, and MTFP1, in kidneys of TFK mice. Our study provides valuable information on the molecular functions and the regulatory network of Tmod1 gene in kidney, as well as the new mechanisms for the regulation of water balance.
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PMID:Quantitative proteomics reveals TMOD1-related proteins associated with water balance regulation. 3133 16


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