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 patient with small cell carcinoma of the lung developed asymptomatic autonomic neuropathy, inappropriate antidiuretic hormone (ADH) secretion and Lambert Eaton myasthenic syndrome. The autonomic neuropathy and inappropriate ADH secretion were present at the time of diagnosis of the tumour. Following chemotherapy these resolved, but 5 months later the patient developed Lambert Eaton syndrome which responded to 3,4-diaminopyridine. This sequence of changes appears to be unique.
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PMID:Lambert Eaton syndrome: autonomic neuropathy and inappropriate antidiuretic hormone secretion in a patient with small cell carcinoma of the lung. 217 71

The blood pressure changes and behavior of vasoactive hormones after various stimuli were studied in eighteen patients with end-stage renal disease maintained on chronic hemodialysis. Group A patients (n = 9) were not subject to intra- or post-dialysis hypotensive episodes, and Group B (n = 9) frequently had such episodes. A 500 ml hypertonic saline infusion produced no change in blood pressure in either group, despite significant rise of vasopressin levels in both. Plasma renin activity levels were similar and became appropriately suppressed by the infusion in both groups, whereas norepinephrine rose significantly only in Group A, but not Group B where it was already higher at baseline. The regular dialysis session produced, as expected, a significantly more profound hypotensive effect in Group B, but was accompanied in both groups by decrease in vasopressin and increase in plasma renin activity. Norepinephrine change differed in the two groups: it decreased in Group A as expected from its capacity to be dialyzed, but rose in several hypotensive patients in Group B, indicating appropriate response to baroreceptor stimulation and leading to an unchanged average. These findings suggest that dialysis-induced hypotensive episodes are not necessarily associated with autonomic neuropathy or with abnormal patterns of vasopressor hormone response to stimuli. They also shed new light on the factors regulating vasopressin secretion under these circumstances, since they indicate that the osmoreceptor and/or sodium-sensitive receptor may be a more dominant mechanism in the regulation of vasopressin release than the volumetric mechanism responding to fluid volume changes.
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PMID:Vasopressin in end-stage renal disease: relationship to salt, catecholamines and renin activity. 330 33

In 83 diabetic patients (23 of them were insulin-dependent) and 34 healthy subjects the influence of water immersion (WI) for 2 hrs on plasma renin activity (PRA), plasma aldosterone and vasopressin (AVP) level was examined. In both examined groups WI exerted a suppressive effect on PRA, plasma aldosterone and AVP level. In this respect only quantitative but not qualitative differences between diabetics and normals were observed. Presence of moderately advanced diabetic nephropathy and autonomic neuropathy influenced only slightly WI induced alterations of the renin-aldosterone system and AVP secretion. In all diabetic patients a defective volumetric mechanism of both the renin-aldosterone system and AVP secretion was stated. In addition in diabetic patients with late diabetic complications a defective osmotic mechanism of AVP secretion was observed. These findings suggest participation also of factors other than hypervolemia and decrease of the plasma osmolality in the mechanism of the observed WI induced suppression of the renin-angiotensin system and AVP secretion in diabetic patients.
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PMID:[Effect of water immersion on plasma renin activity, vasopressin and aldosterone level in diabetics]. 331 Apr 25

The arginine-vasopressin (AVP) response to supine-standing postural change was evaluated in eight healthy subjects and in fourteen diabetic patients. Plasma AVP levels were found to increase in the controls and in nine subjects from the diabetic group. In the controls the increase was 139% 5 min. after standing and 275% 120 min. after standing. In four of the diabetics affected by autonomic neuropathy AVP failed to increase in response to standing, thus suggesting lesions of the neurogenic pathways connecting baroreceptors to neurohypophysis. Consequently, a failure of the afferent limb in the baroregulatory system must be taken into account among other localizations of autonomic neuropathy. On this basis, AVP measurement both in supine and erect positions could represent an additional test for assessing the integrity of the autonomic nervous system.
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PMID:Arginine-vasopressin response to supine-erect posture change: an index for evaluation of the integrity of the afferent component of baroregulatory system in diabetic neuropathy. 369 28

To evaluate the role of vasopressin (AVP) on blood pressure (BP) in diabetic patients with autonomic neuropathy (AN), 10 patients were studied on a fixed sodium and potassium diet. On days 4 and 7, a 24-h BP monitoring, as well as blood and urine samples for sodium, potassium, creatinine, and osmolality determinations were obtained for every 4-h period; either placebo or an AVP-V1-antagonist (d(CH2)5Tyr(me)AVP; 0.5 mg; AVPi) were given iv at 1 PM. On placebo, systolic BP (SBP) showed a progressive elevation during the day, declining after 12 PM (8 AM to 12 AM 122+/-9; 12 AM to 4 PM 125+/-11; 4 PM to 8 PM 134+/-14; 8 PM to 12 PM 136+/-14; 12 PM to 8 AM 131+/-17 mm Hg). On AVPi this rise in SBP was blunted: 8 AM to 12 AM 125+/-122; 12 AM to 4 PM 121+/-21; 4 PM to 8 PM 126+/-16; 8 PM to 12 PM 129+/-14; 12 PM to 8 AM 124+/-12 mm Hg. Creatinine clearance and diureses were greater during the night, both with placebo and AVPi. Plasma osmolality did not change on either day, although serum sodium decreased after AVPi, reaching the lowest values at 4 PM to 8 PM period (137+/-4.7 v 131+/-3.8 mEq/L; P < .05). With placebo, fractional excretion of sodium (FENa) increased from 0.43%+/-0.32% during 12 h of orthostasis to 0.92%+/-1.05% during 12 h of recumbency (P < .02). With AVPi, the FENa on orthostasis did not differ from that with placebo, although BP values were lower and did not increase with recumbency (0.58+/-0.57 v 0.73%+/-0.49%; NS). In conclusion, our results show that in diabetic patients with AN, vasopressin participates in BP control by stimulating vascular and renal V1 receptors, which results in vasoconstriction and sodium reabsorption.
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PMID:Role of vasopressin in 24-hour blood pressure regulation in diabetic patients with autonomic neuropathy. 1182 59

The occurrence of DIH is 15-30 or even 50% of dialysis sessions. There are three clinical patterns of DIH: acute, recurrent and chronic. Intradialytic hypotension essentially augments mortality due to hypoperfusion and concomitant damage of many vital organs, as well as due to chronic overhydration and inability to reach proper dry weight. The main causes of dialysis induced hypotension are age hypovolemia (rapid ultrafiltration), and coexisting decreases: autonomic neuropathy, cardiovascular diseases, diabetes. Therapeutic strategies include: patient education and perfect supervision by dialysis staff dialysis procedure-related methods (extension of dialysis duration, low dialysate temperature, sodium and ultrafiltration profiling and usage of biofeedback technique) and pharmacological treatment (e.g. midodrine, caffeine, vasopressin analogues). Proper treatment includes usage of invasive or cardiosurgical methods of heart failure which is a common reason of hypotension in the dialyzed population. Dialysis-induced hypotension is a very important, multifactorial clinical problem in dialysotherapy. Its incidence increases because of the growing number of elderly and diabetic patients in the dialyzed population.
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PMID:Dialysis induced hypotension--a serious clinical problem in renal replacement therapy. 1892 50

Hyperdynamic circulation in patients with liver cirrhosis is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure and currently focused on understanding the pathogenesis because of possibility of developing novel treatment modality. Basically, these hemodynamic alternations arise from portal hypertension. Portosystemic collaterals develop to counterbalance the increased intrahepatic vascular resistance to portal blood flow and induce an increase in venous return to heart. Increased shear stress in vascular endothelial cell related high blood flow by portosystemic shunting contributes to this upregulation of eNOS resulting in NO overproduction. Additionally, bypassing through portosystemic collaterals and escaping degradation of over-produced circulating vasodilators in the diseased liver can promote the peripheral arterial vasodilation. Vasodilation of the systemic and splanchnic circulations lead to a reduced systemic vascular resistance, and increased cardiac output and splanchnic blood flow. Furthermore, neurohumoral vasoconstrictive systems including systemic nervous system, rennin angiotensin aldosterone system, and vasopressin are intensively activated secondary to vasodilation. However, hyperdynamic circulation would be more aggravated by the activated vasoconstrictive systems. With the progression of the cirrhotic process, hyperdynamic alternations can be more profound due to hyporesponsiveness to vasoconstrictors and increased shunt formation in conjunction with autonomic neuropathy. Eventually, splanchnic arterial vasodilation results in an increase portal venous inflow, maintaining the elevated portal venous pressure. Hyperdynamic circulation is intimately involved in portal hypertension with liver cirrhosis, therefore it is reasonable to have an interest in complete understanding of the pathogenesis of hyperdynamic circulation to develop novel treatment modality.
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PMID:[Hyperdynamic circulation in patients with liver cirrhosis and portal hypertension]. 1984 49

The response of arginin-vasopressin (AVP) to baroreceptor activation (tilt testing) was investigated in patients with diabetic autonomic neuropathy (DAN). The present data show that hypothension induced by upright position showed a slight increase of AVP in patients with DAN in comparison with normal subjects and diabetic patients without DAN. These findings suggest that the blunted AVP response to hypothension may be due to lesions of afferent autonomic pathways present in DAN and plays a role in the pathogenesis of postural hypothension.
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PMID:Vasopressin release induced by hypothension is blunted in patients with diabetic autonomic neuropathy. 2037 May 55

Background: Clozapine is the antipsychotic of choice for treatment-resistant schizophrenia and has minimal risk for extrapyramidal symptoms. Therapeutic benefits, however, are accompanied by a myriad of cardiometabolic side-effects. The specific reasons for clozapine's high propensity to cause adverse cardiometabolic events remain unknown, but it is believed that autonomic dysfunction may play a role in many of these. Objective: This systematic review summarizes the literature on autonomic dysfunction and related cardiovascular side effects associated with clozapine treatment. Method: A search of the EMBASE, MEDLINE, and EBM Cochrane databases was conducted using the search terms antipsychotic agents, antipsychotic drug*, antipsychotic*, schizophrenia, schizophren*, psychos*, psychotic*, mental ill*, mental disorder*, neuroleptic*, cardiovascular*, cardiovascular diseases, clozapine*, clozaril*, autonomic*, sympathetic*, catecholamine*, norepinephrine, noradrenaline, epinephrine, adrenaline. Results: The search yielded 37 studies that were reviewed, of which only 16 studies have used interventions to manage cardiovascular side effects. Side effects reported in the studies include myocarditis, orthostatic hypotension and tachycardia. These were attributed to sympathetic hyperactivity, decreased vagal contribution, blockade of cholinergic and adrenergic receptors, reduced heart rate variability and elevated catecholamines with clozapine use. Autonomic neuropathy was identified by monitoring blood pressure and heart rate changes in response to stimuli and by spectral analysis of heart rate variability. Metoprolol, lorazepam, atenolol, propranolol, amlodipine, vasopressin and norepinephrine infusion were used to treat tachycardia and fluctuations in blood pressure, yet results were limited to case reports. Conclusion: The results indicate there is a lack of clinical studies investigating autonomic dysfunction and a limited use of interventions to manage cardiovascular side effects associated with clozapine. As there is often no alternative treatment for refractory schizophrenia, the current review highlights the need for better designed studies, use of autonomic tests for prevention of cardiovascular disease and development of novel interventions for clozapine-induced side effects.
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PMID:Clozapine-Induced Cardiovascular Side Effects and Autonomic Dysfunction: A Systematic Review. 2967 May 4