Raised plasma arginine vasopressin concentration in carbamazepine-induced water intoxication (original) (raw)
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Dose-response effects of pressor doses of arginine vasopressin on renal haemodynamics in the rat
The Journal of Physiology, 1988
1. Dose-response effects of arginine vasopressin on renal haemodynamics were studied in conscious and in pentobarbitone-anaesthetized rats infused with 77 mm-NaCl at 5-2 and 2X6 ml h-1 respectively. 2. Vasopressin at 0X8 pmol h-1 (100 g body weight)-' did not have a significant effect on arterial blood pressure in conscious or anaesthetized rats. Increasing the dose to 2-5 pmol h-1 (100 g body weight)-' induced a pressor effect in conscious rats but not in anaesthetized rats. A pressor response was observed in the latter at a dose of 10 pmol h-1 (100 g body weight)-'. 3. Pressor doses of vasopressin of 100 pmol h-1 (100 g body weight)-' and less did not significantly alter the clearance of p-aminohippurate (PAH) in either conscious or anaesthetized rats. A dose of 1000 pmol h-1 (100 g body weight)-' significantly decreased PAH clearance in both conscious and anaesthetized animals. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin in both conscious and anaesthetized rats. Moderately pressor doses decreased inulin clearance in conscious animals only. The highest dose administered (1000 pmol h-1 (100 g body weight)-') decreased inulin clearance in both conscious and anaesthetized rats. 5. Pressor doses of vasopressin had a biphasic effect on the filtration fraction in conscious rats. The filtration fraction decreased with doses of vasopressin at the lower end of the pressor range but increased with the highest dose of 1000 pmol h-1 (100 g body weight)-'. In contrast the filtration fraction did not change significantly with moderate pressor doses in anaesthetized rats but was increased by doses of 100 and 1000 pmol h-1 (100 g body weight)-'. 6. It is concluded that pressor doses of vasopressin lower than 100 pmol h-' (100 g body weight)-' do not decrease renal plasma flow rate in conscious or pentobarbitone-anaesthetized rats. The results suggest that the inconsistent effects of vasopressin on renal blood flow reported in the literature are due, at least in part, to the wide range of doses used.
Clinical Endocrinology, 1986
A cytochemical assay has been developed to measure human plasma arginine vasopressin. It is based on the stimulation of Na+-K+, ATPase activity located in the outer medulla of the rat kidney, and is capable of detecting very low plasma arginine vasopressin concentrations, limit of detection 0·01 pmol/l. Specificity for vasopressin stimulation of the enzyme is conferred on the assay by the use of specific vasopressin antiserum. Index of precision of the assay is 0·21. Degradation of arginine vasopressin in plasma in inhibited by phenanthro-line. Samples may be stored up to 8 weeks at - 70°C. Intra- and inter-assay coefficients of variation were 22% (n= 8) and 104% (n=12), respectively. A sustained water load in eight healthy male adults caused a fall in plasma osmolality from a basal of 286·5±2·0 (mean±SEM) to 279·2 ± 2·4 mmol/kg after the load (P> 0.001), which was associated with a reduction in urine osmolality from 867 ± 54 to 69 ± 3 mmol/kg. Plasma immunoreactive arginine vasopressin fell from 1·3 ± 0·3 pmol/l to become undetectable (<0.3 pmol/l), but plasma cytochemical arginine vasopressin decreased from 0·96 ± 0·14 to 0.07 ± 0.02 pmol/l. There was a curvilinear relationship between plasma osmolality and plasma cytochemical arginine vasopressin, which militated against the concept of an osmotic threshold for vasopressin release.
Hypokalemia, glucose intolerance, and hyperinsulinemia during diuretic therapy
Hypertension, 1992
Hypokalemia and glucose intolerance may result from diuretic therapy. Increases in plasma insulin and glucose levels have been observed in thiazide-treated hypertensive patients and have been attributed to a diminished insulin sensitivity induced by diuretic therapy. To investigate the effects of hypokalemia on glucose tolerance and insulin secretion, we studied 21 essential and nine diabetic hypertensive patients after 4 weeks of placebo and after 4 weeks of chlorthalidone therapy (25 mg/day). Plasma glucose and insulin levels were measured for a 3-hour period after a 75-g glucose oral dose. Hypokalemia developed in seven of the essential hypertensive patients (HK group), whereas only one diabetic patient had decreased plasma potassium levels to below 3.5 meq/1. The results obtained in the HK group after chlorthalidone showed that plasma glucose and insulin values increased after the oral glucose load to levels significantly higher than those observed after placebo. In contrast, the patient who remained normokalemic after chlorthalidone did not show any change in plasma insulin and glucose levels during glucose tolerance testing. These results show that diuretic therapy may induce hyperglycemia and hyperinsulinemia and suggest that potassium depletion is involved in the increase in insulin resistance that has been demonstrated during thiazide therapy. {Hypertension 1992;19[suppl II]:II-26-II-29) T he thiazide diuretics are currently the most widely used initial therapy in essential hypertensive patients, and their adverse effects on glucose homeostasis are well documented. 1-2 They are known to impair glucose tolerance in nondiabetic humans and have been involved in the progression from impaired glucose tolerance to overt diabetes. 3 Several mechanisms have been proposed to explain the impairment in carbohydrate metabolism during thiazide therapy. Hypokalemia has been implicated in the deterioration of glycemic control during thiazide therapy, because adequate potassium supplementation has been shown to restore glucose tolerance to pretreatment levels. 4-5 More recently, some reports have demonstrated that the increases in plasma glucose levels consequent to diuretic therapy during glucose tolerance tests are associated with increases in plasma insulin values. 6-7 These observations suggest a decreased tissue sensitivity to insulin as the causative factor of thiazide-induced glucose intolerance. However, a role for potassium depletion in the development of a diuretic-related impairment in peripheral glucose uptake and hyperinsulinemia has not been established.
Acute Effect of Physiological Concentrations of Vasopressin on Rat Renal Function
Clinical and Experimental Pharmacology and Physiology, 1993
1. The antidiuretic, pressor and electrolyte transport effects of arginine vasopressin (AVP) were simultaneously evaluated in the anaesthetized water diuretic rat. Increasing concentrations of AVP (7.5, 75 and 750 ng/ kg bolus and per h), were used to produce plasma levels which approximate the physiological range (4.8 f2.4,35.7 f 12.5, 85.2f 16.1 pg/mL respectively).
Pharmacotherapy, 2011
Study Objectives. To determine whether vasopressin is detectable in the continuous venovenous hemodialysis (CVVHD) effluent of patients receiving exogenous arginine vasopressin, and to determine whether treatment-specific factors are associated with vasopressin levels in CVVHD effluent. Design. Prospective observational study. Setting. Intensive care units of a tertiary care academic medical center. Patients. Twenty-seven adults with vasodilatory shock who received a stabledose continuous intravenous infusion of arginine vasopressin with concomitant uninterrupted CVVHD for at least 4 hours between September 2008 and May 2010. Measurements and Main Results. Vasopressin levels in CVVHD effluent were assessed by radioimmunoassay. Statistical analysis was performed with analysis of variance and Pearson correlation. A multivariate linear regression was used to assess for independent factors associated with vasopressin levels in CVVHD effluent. The CVVHD effluent of all patients was assessed for vasopressin levels. The median exogenous arginine vasopressin dose was 0.03 unit/minute (range 0.02-0.18 unit/min), whereas the median CVVHD effluent flow rate was 22.6 ml/kg/hour (interquartile range [IQR] 21.5-26.8 ml/kg/hr). Vasopressin was detectable in all effluent samples (median 88.8 pg/ml, IQR 36.4-113.7 pg/ml). There were no significant differences in CVVHD effluent vasopressin levels among CVVHD filter types (p=0.39). The CVVHD effluent vasopressin levels correlated with exogenous arginine vasopressin dose (r 2 =0.49, p<0.001). After adjustment for CVVHD effluent flow rate and administration of corticosteroids, with multivariate linear regression, only exogenous arginine vasopressin dose was independently associated with CVVHD effluent vasopressin level. Conclusion. Vasopressin is detectable in CVVHD effluent, suggesting that it is removed by CVVHD. In addition, exogenous arginine vasopressin infusion dose is independently associated with CVVHD effluent vasopressin level.
Vasopressin Excess and Hyponatremia
American Journal of Kidney Diseases, 2006
is a common electrolyte disorder that frequently is overlooked and undertreated. Although the pathophysiological process of hyponatremia is complex, arginine vasopressin (AVP) is a common etiologic factor. Excess AVP release by osmotic or nonosmotic stimuli or both can lead to sodium and water imbalance. Conventional treatment options for hyponatremia, including water restriction and administration of sodium chloride with or without loop diuretics, do not directly address the underlying water retention induced by excess AVP in many cases. Clinical trials showed that AVP-receptor antagonists, including lixivaptan, tolvaptan, and conivaptan, produce aquaresis, the electrolyte-sparing excretion of free water, to correct serum sodium concentration. We review results from recent clinical trials involving AVP-receptor antagonists in the treatment of hyponatremia associated with AVP excess.
Metabolic clearance rate of immunoreactive vasopressin in man
European Journal of Clinical Investigation, 1982
Metabolic clearance of synthetic arginine vasopressin (AVP) has been measured in sixteen healthy subjects and ten uraemic patients on maintenance haemodialysis. Plasma AVP was measured using a specific radioimmunoassay at different intervals after a single injection of 2 pg AVP. The theoretical curve which fitted best with the disappearance curve was the sum of two exponentials in twenty-two subjects and of three exponentials in the other four. Metabolic clearance rate and the volume of fast initial distribution were 287.1 ml min-* (m2)-I and 219.3 ml/kg b.w., respectively, in normal subjects. Metabolic clearance rate was considerably lower in the uraemic group. This emphasizes the role of kidneys in the degradation of AVP and may account, at least in part, for the higher basal plasma value of this hormone observed in uraemic patients.