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)

Clonidine s.c. (0.01-0.3 mg/kg), in unanesthetized rats, caused an initial rise (+20 mm Hg), followed by a continuous fall of BP and a dose-dependent natriuresis and diuresis for up to 2 h. Glomerular filtration rate (GFR) (CIn) increased during the first 20 min, while effective renal plasma flow (ERPF) (CPAH) remained normal. Subsequently, between 20 and 60 min after injection, ERPF (CPAH) decreased considerably while GFR had reverted to its normal value. In saline-infused rats clonidine diuresis was accompanied by an "inappropriate" positive free water clearance. Pentobarbital anesthesia suppressed the initial BP peak and the diuresis. Phenoxybenzamine (1 mg/kg i.v.) was antinatriuretic in saline diuresis; the effect of phenoxybenzamine + clonidine on diuresis and salt excretion represented the sum of the effects of both drugs, but phenoxybenzamine enhanced the clonidine-induced increase of GFR. Neither haloperidol (1 mg/kg i.v.) nor bulbocapnine (3 mg/kg i.v.) interfered with the renal effects of clonidine. Clonidine s.c. caused hyperglycemia and glucosuria which did not account for the natriuresis. Clonidine thus appears to increase the GFR and "filtration fraction" (FF) by a phenoxybenzamine-insensitive rise of glomerular ultrafiltration, to depress ERPF by alpha-adrenergic afferent vasoconstriction, to induce natriuresis by a tubular action not blocked by phenoxybenzamine and to exert an antivasopressin effect, either by depressing pituitary vasopressin secretion or the renal response to vasopressin.
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PMID:The renal effects of clonidine in unanesthetized rats. 4 24

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.
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PMID:Plasma vasopressin in uncontrolled diabetes mellitus. 10 67

An experiment was performed in female rats in order to assess the influence and mechanism underlying the effects of hyperglycemia, hypertonic saline and vasopressin upon the gastric acid secretion and mucosal blood flow (MBF). Infusion of isotonic saline did not alter acid output and gastric clearance of plasma aminopyrine whereas hypertonic solutions (20% glucose or 3% NaCl) significantly increased plasma osmolality and decreased the acid secretion within 30 min and recovered to normal levels after 2 h. Vasopressin also effectively inhibited acid secretion. Both hypertonic solutions and vasopressin decreased the mucosal blood flow. However, the ratio (R) of MBF to gastric secretory rate which is a helpful guide to the mechanism of secretory inhibition did not significantly change in either case. We concluded that all three agents probably had a direct action on secretion rather than decreasing MBF. The mechanism of inhabition of acid secretion and its relationship to MBF was suggested and discussed.
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PMID:Mechanism of inhibition of gastric acid secretion by hypertonic solutions and vasopressin. 103 18

Metabolic effects of vasopressin, glucagan and adrenalin were compared, in intact rats, especially in regard to time courses of effects. Hyperglycaemia was transient in response to vasopressin, prolonged following adrenalin, and, suprisingly, was not discernible after glucagon, except in response to a very large dose. Vasopressin decreased and adrenalin increased, the plasma free fatty acid concentration; both hormones decreased the triacylglycerol level. Muscle glycogen concentrations, measured in heart, diaphragm and skeletal muscle, exhibited small changes, with complex time courses, following hormone administration. Vasopressin brought about a rapid but transient activation of heaptic glycogen phosphorylase which resembled that due to adrenalin. The activation by glucagon of phosphorylase was greater and more prolonged, despite the absence of hyperglycaemia. In response to vasopressin, there was in increase in plasma insulin. Incorporation of 14C from [14C]glucose into glycogen or fatty acids was not influenced by vasopressin. Taken together, these results may be explained by rapid metabolic action of vasopressin on hepatic glycogenolysis, whereas adrenalin has multiple prolonged actions.
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PMID:Metabolic actions of vasopressin, glucagon and adrenalin in the intact rat. 118

Trapymin (TM) relaxed excised renal, coronary, pulmonary, femoral and mesenteric arteries and this relaxation was not antagonized by propranolol. The dose-response curve of TM was parallel to that of nitroglycerin and papaverine and steeper than that of dipyridamol or adenosine. TM exerted inotropic and chronotropic actions on excised rat atrium. TM was also effective through the oral route and the effectiveness tended to decrease slightly after repeated use for ten days. TM was effective on vasopressin induced angina in rats and electrocoagulation-induced myocardial infarction. TM suppressed adrenaline-induced arrhythmia but not CaCl2-induced arrhythmia. TM reduced catecholamine content in brain, adrenals and heart but had no influence on monoamine oxidase or dopamine-beta-hydroxylase. TM revealed ganglion-blocking and neuron-blocking actions in cervical ganglion in cats. With propranolol, TM-induced hyperglycemia and reduction in glycogen content in liver and heart was antagonized but TM-induced rise in free fatty acid in serum was not antagonized. Na+-K+ dependent ATPase of bovine heart and P/O ratio of mitochondria of rat heart was not influenced by TM. ADP-induced aggregation of platelets was antagonized by TM. These data indicate that TM induced coronary dilation is partly due to a papaverine like action and also to ganglion-blocking, neuron-blocking and anti-adrenergic action. On the other hand, TM possessed catecholamine release and cardiotonic action as related to beta-receptors.
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PMID:[Pharmacology of cornary dilator agent, trapymin. (2) Analysis of its mode of action]. 124 70

Blood glucose, plasma sodium, bicarbonate (HCO3-), vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3- (r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P less than 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.
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PMID:Correlates of brain edema in uncontrolled IDDM. 156 33

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

Previous reports have described 5-20% prevalence of hyponatremia in extended care facilities, due largely to drugs or inappropriate antidiuretic hormone secretion. In our 400 bed VA extended care facility, 15 men with organic brain syndrome (Alzheimer's, multi-infarct dementia, anoxic encephalopathy or alcoholism) currently receive Isocal via gastrostomy as the sole source of nutrition. We noted intermittent hyponatremia in about half of these patients, and conducted a chart review to investigate the cause. Mean age was 68 yr (range 46-92); tube feeding duration was 3 mo.-3 yr; 266 Na concentrations were obtained from the charts. Simultaneous with these Na analyses, one of three diets prevailed: (A) mixed foods (3-6 g Na/day) orally before gastrostomy; (B) Isocal supplemented with NaCl to give 2 g Na/day; (C) unsupplemented Isocal providing 1 g Na/day. (B) and (C) had been randomly varied by rotating physicians. Serum Na was directly related to Na intake. On (A), Na was within normal range (135-145 mEq/l) in all men. One patient was hyponatremic during diet (B). During (C), eight patients were hyponatremic. Na was less than 135 mEq/l in 40% of all samples during diet (C) and less than 130 mEq/l in 14%. Changing from diet (A) or (B) to diet (C) caused nearly equivalent declines in Na and Cl; K and HCO-3 were unaffected. No hyponatremic patient took drugs known to cause hyponatremia, or had congestive heart failure, hypoalbuminemia, lipemia or fasting hyperglycemia. At the end of the study, four hyponatremic men were changed from (C) to (B); serum Na became normal in all four patients, without edema or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremia in tube-fed elderly men. 308 Apr 61

In most diabetic patients, the presence of hyponatremia is usually ascribed to severe hyperglycemia, hypertriglyceridemia, oral hypoglycemic agents, or other drugs. We describe two insulin-treated type II diabetic patients who were seen with severe rapid weight loss, hyponatremia, and diabetic amyotrophy despite good metabolic control. Laboratory evaluation of the hyponatremia suggested the syndrome of inappropriate antidiuretic hormone secretion. Their clinical presentations led to the suspicion of an underlying malignant neoplasm in each case. One patient required demeclocycline for treatment of his symptomatic hyponatremia, while the other improved with fluid restriction and intermittent furosemide therapy. The hyponatremia resolved spontaneously with improvement in body weight and the amyotrophy resolved after four to six months. After 24 to 36 months of close follow-up, no evidence of malignancy has been documented in either of the patients. We conclude that this clinical entity of amyotrophy is benign and should be included in the differential diagnosis of chronic hyponatremia in diabetic patients.
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PMID:Chronic hyponatremia associated with diabetic amyotrophy. 308 5

Corticotropin-releasing factor (CRF) has been identified in brain regions that participate in the regulation of the autonomic nervous system and behavioral responses. This paper summarizes the central nervous system as well as the peripheral effects of CRF that are different from those on the anterior pituitary. CRF acts within the brain to increase plasma concentrations of adrenaline and noradrenaline resulting in increased plasma concentrations of glucagon and in hyperglycemia. In the dog, CRF also acts within the brain to increase plasma concentrations of vasopressin. The intracerebroventricular administration of CRF results in a decrease of gastric acid secretion stimulated exogenously by pentagastrin and 2-deoxy-D-glucose or stimulated endogenously by a protein meal. CRF also acts within the brain to decrease gastric emptying and small intestinal transit but to increase large bowel transit and fecal excretions. The central administration of CRF produces hypertension, tachycardia and an elevated oxygen consumption. The effects of CRF on behavior are numerous. CRF induces a reduction in food intake, increases grooming behavior, locomotor activity, vocalization and induces an aroused state but decreases sexual receptivity. Intravenous administration of CRF decreases gastric acid secretion, gastric emptying and blood pressure but increases heart rate, plasma vasopressin concentrations, mesenteric and aortic blood flow, venous return to the heart and pancreatic bicarbonate and protein secretions. The physiological significance of these peripheral actions of CRF on various organ systems is not known.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrapituitary effects of corticotropin-releasing factor. 332 96


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