Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 71-year-old female with amyotrophic lateral sclerosis (ALS) developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during respiratory failure due to atrophy of the respiratory muscles. Serum sodium concentration fell to 116 mEq/l and then returned to the normal range after water restriction and respiratory care. This is considered to be the first case report of ALS associated with SIADH.
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PMID:Amyotrophic lateral sclerosis associated with the syndrome of inappropriate secretion of antidiuretic hormone. 147 61

We studied trophic effects of angiotensin II, vasopressin, cholecystokinin, and oxytocin on explanted ventral spinal cord cultures from 13- and 14-day-old rat embryos. There was a significant neurite promoting effect of the spinal cord cultures by using angiotensin II, vasopressin, and cholecystokinin. Cholecystokinin had the most potent effect at any concentrations. The minimum effective concentration was 10(-8) M in angiotensin II and vasopressin and 10(-12) M in cholecystokinin, respectively. The effect of angiotensin II and vasopressin was dependent on concentrations. However, the rate and grade of neurite appearance did not correlate with the concentrations of cholecystokinin. Oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II, vasopressin and cholecystokinin have neurotrophic effects on the ventral spinal cord in cultures, and may be candidates for therapeutic trials of amyotrophic lateral sclerosis.
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PMID:Trophic effect of angiotensin II, vasopressin and other peptides on the cultured ventral spinal cord of rat embryo. 188 May 32

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures derived from 13 to 14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8)M in both angiotensin II and vasopressin. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:[Trophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo]. 227 65

Ten patients with amyotrophic lateral sclerosis were treated during 5 consecutive days with intravenous infusion of high-dose human leukocyte interferon-alpha (IFN-alpha) or placebo in a single-blinded randomized trial. To assess the effect of IFN on the water and electrolyte balance, serum electrolytes, creatinine, and antidiuretic hormone as well as urine excretion of electrolytes, aldosterone, and cortisol were measured before the trial and during the fourth day of IFN infusion. Compared with placebo the results showed a significant reduction of the mean serum calcium level (from 2.28 +/- 0.03 mmole/liter to 2.01 +/- 0.06 mmole/liter; p less than 0.01), that of the mean serum osmolality (from 296 +/- 9.9 mosm/kgH2O to 281 +/- 2.5 mosm/kgH2O; p less than 0.05) and that of the mean urinary excretion of magnesium (from 5.32 +/- 2.04 mmoles/liter to 2.65 +/- 1.68 mmoles/liter; p less than 0.05). Careful observation of water and electrolyte balance is emphasized during high-dose IFN treatment.
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PMID:Disturbance of the water and electrolyte balance during high-dose interferon treatment. 234 51

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures from 13-14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8) M in angiotensin II and vasopressin respectively. Effect of these two neuropeptides was concentration-dependent. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:Neurotrophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo. 258 29

6 patients with amyotrophic lateral sclerosis were treated with intravenous infusion of 100-200 million IU per day of human leukocyte interferon. Side effects of treatment included fever, chills, malaise, nausea, marked leukopenia, mild anemia, and thrombocytopenia. Tiredness, confusion, papilledema, and overall signs of acute encephalitis were observed. Tendon reflexes and muscle force decreased. EEG activity was slowed, and evoked potentials showed significant slowing of conduction times. Neuropsychological tests revealed congitive dysfunction. The syndrome of inappropriate antidiuretic hormone secretion developed in all patients. All side effects were reversible with cessation of interferon treatment.
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PMID:Neurotoxic and other side effects of high-dose interferon in amyotrophic lateral sclerosis. 620 81

Amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disorder of the motor system in the CNS characterized by motor neuron death in the spinal cord, brain stem and cortex. Readily available tissues such as fibroblasts from ALS patients can serve as simple model systems to study the molecular mechanisms leading to degenerative disorders. We have used Fura-2 fluorescence microscopy and single-cell imaging to study the spatiotemporal dynamics of intracellular free calcium ([Ca2+]i) in primary cultures of fibroblasts from skin biopsies from ALS and normal subjects. Increases in [Ca2+]i were induced by stimulation with bradykinin (100 nM); neurotensin (50 nM); N-formyl-Met-Leu-Phe (chemotactic peptide) (1 microM); [Arg8]-vasopressin (1 microM) and histamine (10 microM). The levels of [Ca2+]i in 80-120 individual cells per agonist were monitored for 15 min. No significant differences were found in the resting levels of [Ca2+]i in control (102 +/- 4 nM) and ALS (98 +/- 6 nM) fibroblasts and in the maximal [Ca2+]i levels after stimulation with N-formyl-Met-Leu-Phe, [Arg8]-vasopressin, and histamine. Significantly lower [Ca2+]i transients were found in fibroblasts from ALS donors compared to controls when stimulated with neurotensin (p < 0.002) and bradykinin (p < 0.005). The percentage of individual cells reacting to a given agonist (40-100%) was similar in both groups. The molecular basis of the impaired calcium homeostasis in fibroblasts from ALS patients is not known, but a generalized membrane defect can be excluded since the [Ca2+]i responses are defective only when bradykinin or neurotensin are used as agonists.
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PMID:Calcium homeostasis in fibroblasts from patients with amyotrophic lateral sclerosis. 785 28

We report 2 autopsy-proven cases of motor neuron disease/amyotrophic lateral sclerosis (MND/ALS), who developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) prior to the respiratory failure. With respect to the underlying mechanisms of SIADH in the cases, we considered two factors; 1) dysfunction of the feedback system in ADH secretion via intrathoracic volume receptors caused by changes in intrathoracic circulation, and 2) primarily functional abnormalities in the limbic system which could influence hypothalamic osmoreceptors. It appears that SIADH can be followed by an exacerbation of respiratory dysfunction in MND/ALS.
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PMID:Two cases of MND/ALS developing the syndrome of inappropriate secretion of antidiuretic hormone. 932 81

In this study, we examined the effects of oxidative stress on a nitric oxide (NO)-regulated neuroendocrine function, the release of arginine vasopressin (AVP) by the hypothalamo-neurohypophyseal axis. Treatment of mouse-isolated hypothalami and neurointermediate lobes (NIL) with H2O2 increased AVP release. This effect was inhibited by copper-zinc superoxide dismutase-1 (SOD1) analogs. By measuring cGMP accumulation as an indicator of biologically active NO, we found that H2O2 treatment decreased cGMP formation in both hypothalami and NIL. We have previously shown that NO inhibits AVP release by a cGMP-independent mechanism. Given that H2O2 stimulated AVP release, while it reduced cGMP production, our findings strongly suggest that oxidative damage affects neurosecretion by reducing NO availability. To test whether such a mechanism may operate under pathological conditions with pronounced oxidative stress, we compared neurosecretion in wild-type and transgenic mice carrying a mutated form of SOD1 associated with human familial amyotrophic lateral sclerosis. Reminiscent of the data obtained from H2O2-treated tissues, hypothalami and NIL from SOD1 mutants displayed decreased cGMP accumulation and increased AVP release, compared with tissues from wild-type littermates. Since neuronal NO synthase expression was not modified, we conclude that the perturbed free radical metabolism associated with the SOD1 mutation is likely to trap NO, and thereby alter neurosecretion, a mechanism that can be exacerbated in specific physiopathological conditions.
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PMID:Oxidative stress and a murine superoxide dismutase-1 mutation promoting amyotrophic lateral sclerosis alter neurosecretion in the hypothalamo-neurohypophyseal axis. 1034 79

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure. 1038 39


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