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Research Highlights from the Literature

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2002; Volume 12(4) from Clinical Autonomic Research                                           
Send comments or suggestions about Autonomic News to: italo.biaggioni@mcmail.vanderbilt.edu

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To review the original abstract of these articles, click on the references below

Welcome any advice, even from a mice?  <<
       
Since the recognition that alpha-synuclein is the most abundant protein in the cytoplasmic inclusions found in Lewy Body diseases and multiple system atrophy, there has been great interest in defining a causal relationship in the pathogenesis of these disorders.  Several transgenic animals overexpressing "-synuclein have been developed for this purpose.  Although cytoplasmic inclusions are formed in most of these animal models, it has been difficult to precisely reproduce the human disease.  The choice of promoter guiding the expression of alpha-synuclein gene may be one of the explanations for this.  Rockenstein et al, found that mice expressing wild type human alpha-synuclein driven by the Thy-1 promoter developed widespread neuronal inclusions throughout the brain.  In contrast, the inclusions that develop in mice expressing "-synuclein driven by the PDGF-beta promoter follow the distribution found in normal brain (neocortex, limbic system and olfactory regions). Inclusions were also found in glial cells, mimicking the pathology of multiple system atrophy. 
        Kahle et al generated transgenic mice expressing wild type human
alpha-synuclein driven by a proteolipid protein promoter.  These animals developed glial inclusions that, in many ways, resembled those found in multiple system atrophy, because the protein was phosphorylated in amino acid S129 and formed detergent-insoluble precipitates.  Despite these histological similarities, no motor abnormalities were observed in these mice, suggesting that other risks factors are required in the pathogenesis of multiple system atrophy. 
        Gisasson et al, generated mice expressing either wild type or A53T mutated human
"-synuclein.  This is the mutation found in many cases of familial Parkinson’s Disease.  Mice expressing mutant, but not wild type, alpha-synuclein, developed a severe and complex motor impairment leading to paralysis and death.  This was associated with the development of age-dependent intracytoplasmatic neuronal inclusions that resemble those seen in familial Parkinson’s Disease.  It would be of interest to determine if autonomic abnormalities are found in these different animal models.
       
Rockenstein E, Mallory M, Hashimoto M et al (2002). Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters. J Neurosci Res 68:568-578.
        Kahle PJ, Neumann M, Ozmen L et al (2002). Hyperphosphorylation and insolubility of {alpha}-synuclein in transgenic mouse oligodendrocytes. EMBO Rep 3:583-588.
        Giasson BI, Duda JE, Quinn SM, Zhang B, Trojanowski JQ, Lee VMY (2002). Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. Neuron 34:521-533.

Imaging; can we see autonomic function and dysfunction?  <<
       
It is often difficult to differentiate between Parkinson’s Disease (PD) and multiple system atrophy with parkinsonian features (MSA-P) early in the disease process.  Bhattacharya et al investigated the usefulness of brain MRI in 21 patients with a clinical diagnosis of PD and 14 with MSA-P.  All patients with MSA-P had abnormal brain MR, characterized by putaminal and brainstem atrophy, and abnormal signal in the middle cerebellar peduncles.  These abnormalities were not seen in PD patients.  Brain imaging, however, may be of limited value in initial MSA-P, as it may show only mild abnormalities.
        It is proposed that the initial autonomic arousal induced by fear and stress, may modulate subsequent conditioning responses.  A way to test for such an interplay is to study subjects with impaired autonomic responses, such as patients with pure autonomic failure.  Critchey et al used this approach coupled with functional MRI.  Fear conditioning was associated with enhanced activity in amygdala and insula.  This activity was reduced in patients with autonomic denervation lacking autonomic arousal.  The authors conclude that fear conditioning is modulated by autonomic arousal.
       
Bhattacharya K, Saadia D, Eisenkraft B et al (2002). Brain magnetic resonance imaging in multiple-system atrophy and Parkinson disease: a diagnostic algorithm. Arch Neurol 59:835-842.
        Critchley HD, Mathias CJ, Dolan RJ (2002). Fear conditioning in humans: the influence of awareness and autonomic arousal on functional neuroanatomy. Neuron 33:653-663.

More on beta-Blockers in the treatment of neurocardiogenic syncope  <<
       
The pathophysiology of neurocardiogenic syncope is still not completely understood.  Not surprisingly, its management remains controversial.  Beta-blockers remain a popular treatment, based on the observation that beta-agonist precipitate tilt-induced syncope, and the hypothesis that myocardial afferents triggering syncope are activated by increased myocardial contractility in the setting of reduced cardiac volume (a beta-mediated effect).  However, there are clinical situations when syncope occurs in the absence of myocardial afferents (e.g., in cardiac transplant patients).  Recent evidence also suggests that epinephrine may be released before syncope, and beta2-mediated vasodilation induced by circulating epinephrine could contribute to syncope.  However, intra-arterial beta-blockade does not prevent syncope-induced forearm vasodilation (see Dietz et al. J Appl Physiol 1997;82:1785).  Dendi and Goldstein used meta-analysis to compare the effectiveness of beta1-selective and non-selective beta-blockers in the treatment of neurocardiogenic syncope.  They compare 19 published studies including a total of 1,060 patients with tilt-induced syncope.  The outcome measure was the percentage of patients in whom syncope was prevented during a subsequent tilt.  Not all studies were randomized or placebo controlled, and the high success rate reported (75-100% prevention of tilt-induced syncope with non-selective $-blockers) arguably suggests that mild cases were included in these trials.  Furthermore, the use of repeat tilt to guide treatment remains controversial.  E.g., in a relatively small study, the efficacy of $-blockers in preventing spontaneous syncope was unrelated to the initial or subsequent response to tilt (see Ventura et al. J Pacing Clin Electrophysiol 2002;25:816).  Nonetheless, using these criteria, meta-analysis showed that non-selective beta-blockers were more effective in preventing tilt-induced syncope. 
        Others have hypothesized that lipophilic
beta-blockers able to reach the CNS (e.g., propranolol) are more effective than hydrophilic ones (e.g., atenolol), suggesting that beta-blockers act centrally to prevent syncope triggering.  Tank et al, studied the central effects of propranolol by measuring muscle sympathetic nerve activity (MSNA) during complete beta-blockade.  At rest, in the supine position, propranolol did not lower blood pressure or altered spontaneous baroreflex slopes, but increased MSNA.  However, the operating points of the parasympathetic and sympathetic baroreflex during beta-blockade were on the baroreflex curves obtained at baseline.  Furthermore, beta-blockade blunted the heart rate increase to the cold pressor test, but not the increase in blood pressure or MSNA.  The authors concluded that the central effects of beta-blockers probably do not play an important role on autonomic regulation.
        Dendi R, Goldstein DS (2002). Meta-analysis of nonselective versus beta-1 adrenoceptor- selective blockade in prevention of tilt-induced neurocardiogenic syncope. Am J Cardiol 89:1319-1321.
        Tank J, Diedrich A, Schroeder C et al (2001). Limited effect of systemic beta-blockade on sympathetic outflow. Hypertension 38:1377-1381.

Impaired arterial vasoconstriction in orthostatic intolerance  <<
       
The pathophysiology of orthostatic intolerance (POTS) is incompletely understood.  Lower limb cyanosis and edema is apparent in these patients, suggesting inappropriate venous pooling.  Other studies have also suggested impaired leg vasoconstriction (see Jacob et al., New Engl J Med 2000;343:1008).  Stewart et al, measured leg blood flow and venous compliance in 15 adolescents with orthostatic intolerance at rest, and in response to 35° head-up tilt, and compared them to 11 healthy controls.  A subset of patients had abnormally high calf venous pressure in the supine position, whereas others had venous pressure comparable to normal controls.  Venous capacitance, and volume/venous pressure relationships were normal in both subsets of orthostatic intolerance patients.  In contrast, the expected leg arterial vasoconstriction produced by upright tilt was not observed in patients with orthostatic intolerance.  Patients with high resting venous pressure had abnormally high leg, but not arm, vascular resistance at rest.  Even in this group, however, vascular resistance did not increase during tilt.  Thus, selective impairment of leg vasoconstriction contributes to the pathophysiology of orthostatic intolerance.  This study also demonstrates that orthostatic intolerance is a heterogeneous disorder.  It is possible that different pathophysiological processes lead to similar clinical presentations.
        Stewart JM (2002). Pooling in chronic orthostatic intolerance: arterial vasoconstrictive but not venous compliance defects. Circulation 105:2274-2281.

You are what you eat? (At least you blood pressure and heart rate are)  <<
       
Ingestion of food, and even water, has a substantial impact on vascular tone, but blood pressure changes are effectively masked by baroreflex mechanisms in normal subjects.  Even modest changes in baroreflex function may have a substantial effects on the sensitivity to vasoactive substances (e.g., see Jordan, et al, Circulation 2002;105:1459).  Thus, in patients with autonomic failure and in the elderly meals can produce a significant decrease in blood pressure and predispose to falls associated to orthostatic hypotension.  To test the hypothesis that the magnitude of postprandial hypotension depends on the rate of nutrient delivered to the duodenum, O’Donovan infused glucose via a duodenal tube at a rate of either 1 or 3 kcal/min in eight healthy elderly subjects.  Only the highest infusion rate decreased blood pressure.  This was associated with a greater rise in blood glucose and plasma insulin.  Postprandial hypotension, therefore, may be less pronounced in patients with delayed gastric emptying.
        Contrary to the effects of meals, acute ingestion of 16 oz of water produces dramatic increases in blood pressure in patients with autonomic impairment.  Shannon et al, reported the potential therapeutic use of water.  Water improved upright blood pressure in autonomic failure patients, from 83/53 to 114/66 mm Hg, and blunted the fall in blood pressure after meals (from -43 to -22 mm Hg systolic blood pressure fall).  It also attenuated the orthostatic tachycardia in patients with orthostatic intolerance (POTS), from 123 to 108 bpm.  Thus, water is an effective adjuvant in the treatment of autonomic disorders.
       
O'Donovan D, Feinle C, Tonkin A, Horowitz M, Jones KL (2002). Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects. J  Physiol 540:673-679.
        Shannon JR, Diedrich A, Biaggioni I et al (2002). Water drinking as a treatment for orthostatic syndromes. Am J Med 112:355-360.


Rockenstein E, Mallory M, Hashimoto M et al (2002). Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters. Journal of Neuroscience Research.68:568-578.

Abstract: Accumulation of alpha-synuclein has been associated with neurodegenerative disorders, such as Lewy body disease and multiple system atrophy. We previously showed that expression of wild-type human alpha-synuclein in transgenic mice results in motor and dopaminergic deficits associated with inclusion formation. To determine whether different levels of human alpha-synuclein expression from distinct promoters might result in neuropathology mimicking other synucleopathies, we compared patterns of human alpha-synuclein accumulation in the brains of transgenic mice expressing this molecule from the murine Thy-1 and platelet-derived growth factor (PDGF) promoters. In murine Thy-1-human alpha-synuclein transgenic mice, this protein accumulated in synapses and neurons throughout the brain, including the thalamus, basal ganglia, substantia nigra, and brainstem. Expression of human alpha-synuclein from the PDGF promoter resulted in accumulation in synapses of the neocortex, limbic system, and olfactory regions as well as formation of inclusion bodies in neurons in deeper layers of the neocortex. Furthermore, one of the intermediate expresser lines (line M) displayed human alpha-synuclein expression in glial cells mimicking some features of multiple system atrophy. These results show a more widespread accumulation of human alpha- synuclein in transgenic mouse brains. Taken together, these studies support the contention that human alpha-synuclein expression in transgenic mice might mimic some neuropathological alterations observed in Lewy body disease and other synucleopathies, such as multiple system atrophy. (C) 2002 Wiley-Liss, Inc

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Kahle PJ, Neumann M, Ozmen L et al (2002). Hyperphosphorylation and insolubility of {alpha}-synuclein in transgenic mouse oligodendrocytes. EMBO Rep.3:583-588.

Abstract: (Oligodendro)glial cytoplasmic inclusions composed of alpha-synuclein (alphaSYN) characterize multiple system atrophy (MSA). Mature oligodendrocytes (OLs) do not normally express alphaSYN, so MSA pathology may arise from aberrant expression of alphaSYN in OLs. To study pathological deposition of alphaSYN in OLs, transgenic mice were generated in which human wild-type alphaSYN was driven by a proteolipid protein promoter. Transgenic alphaSYN was detected in OLs but no other brain cell type. At the light microscopic level, the transgenic alphaSYN profiles resembled glial cytoplasmic inclusions. Strikingly, the diagnostic hyperphosphorylation at S129 of alphaSYN was reproduced in the transgenic mice. A significant proportion of the transgenic alphaSYN was detergent insoluble, as in MSA patients. The histological and biochemical abnormalities were specific for the disease-relevant alphaSYN because control green fluorescent protein was fully soluble and evenly distributed throughout OL cell bodies and processes. Thus, ectopic expression alphaSYN in OLs might initiate salient features of MSA pathology

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Giasson BI, Duda JE, Quinn SM, Zhang B, Trojanowski JQ, Lee VMY (2002). Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. Neuron.34:521-533.

Abstract: alpha-Synucleinopathies are neurodegenerative disorders that range pathologically from the demise of select groups of nuclei to pervasive degeneration throughout the neuraxis. Although mounting evidence suggests that alpha-synuclein lesions lead to neurodegeneration, this remains controversial. To explore this issue, we generated transgenic mice expressing wild-type and A53T human alpha-synuclein in CNS neurons. Mice expressing mutant, but not wild-type, alpha-synuclein developed a severe and complex motor impairment leading to paralysis and death. These animals developed age-dependent intracytoplasmic neuronal alpha-synuclein inclusions paralleling disease onset, and the alpha-synuclein inclusions recapitulated features of human counterparts. Moreover, immunoelectron microscopy revealed that the alpha-synuclein inclusions contained 10-16 nm wide fibrils similar to human pathological inclusions. These mice demonstrate that A53T alpha-synuclein leads to the formation of toxic filamentous alpha-synuclein neuronal inclusions that cause neurodegeneration

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Bhattacharya K, Saadia D, Eisenkraft B et al (2002). Brain magnetic resonance imaging in multiple-system atrophy and Parkinson disease: a diagnostic algorithm. Arch Neurol.59:835-842.

Abstract: BACKGROUND: Brain magnetic resonance (MR) imaging offers the potential for objective criteria in the differential diagnosis of multiple system atrophy with predominant parkinsonism (MSA-P) and Parkinson disease (PD), since it frequently shows characteristic abnormalities in patients with MSA-P and is believed to be normal in patients with PD. OBJECTIVE: To determine concordance between clinical and MR imaging-based diagnoses of MSA-P and PD. DESIGN: Two neuroradiologists identified and rated striatal and infratentorial abnormalities in 39 brain MR images and assigned a diagnosis of PD, MSA-P, or MSA with additional marked cerebellar ataxia (MSA-C). SETTING: Academic medical center. PATIENTS: Thirty-nine patients with parkinsonism, including 21 with a clinical diagnosis of PD, 14 with MSA-P, and 4 with MSA-C. RESULTS: All patients with MSA and 14 (67%) of 21 patients with PD had some abnormality on brain MR imaging. Brainstem atrophy was seen in patients with MSA-P and MSA-C. Putaminal atrophy was seen only in MSA-P. Putaminal hypointensity and lateral slitlike hyperintensity were seen in both PD and MSA-P but were always mild in PD. Cerebellar abnormalities, seen in all patients with MSA-C and 11 patients with MSA-P, were also identified in 6 patients with PD, albeit always rated as mild. Nonconcordance between clinical and radiological diagnosis occurred in 2 patients with PD, 5 with MSA-P, and 1 with MSA-C. CONCLUSION: Since several features on brain MR imaging are seen only in MSA-P, a simple diagnostic algorithm may improve the MR imaging diagnosis of MSA-P and PD

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Critchley HD, Mathias CJ, Dolan RJ (2002). Fear conditioning in humans: the influence of awareness and autonomic arousal on functional neuroanatomy. Neuron.33:653-663.

Abstract: The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal

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Dendi R, Goldstein DS (2002). Meta-analysis of nonselective versus beta-1 adrenoceptor- selective blockade in prevention of tilt-induced neurocardiogenic syncope. American Journal of Cardiology.89:1319-1321.

Abstract: Beta-adrenoceptor blockers are frequently used to treat patients predisposed to neurocardiogenic syncope. Beta-2 adrenoceptor-mediated skeletal vasodilation might contribute to neurocardiogenic syncope, and consistent with this notion, meta-analysis of published reports indicates that nonselective beta blockers are more effective than beta-1-selective blockers in preventing tilt-induced syncope

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Tank J, Diedrich A, Schroeder C et al (2001). Limited effect of systemic beta-blockade on sympathetic outflow. Hypertension.38:1377-1381.

Abstract: Central beta-adrenoreceptors may augment sympathetic outflow. We tested the hypothesis that beta-blockade attenuates central sympathetic outflow by inhibiting central adrenoreceptors. We studied 18 healthy controls (4 female, 14 male; age, 26+/-6 years, body mass index, 23+/-3 kg/m(2)). ECG, brachial, and finger arterial blood pressure, muscle sympathetic nerve activity, and respiration were measured continuously before and during complete beta-blockade. Subjects received a total intravenous dose of 0.21 mg/kg of propranolol in 15 minutes. Spontaneous baroreflex slopes were calculated using the sequence technique (BRSup, BRSdown). The sympathetic baroreflex slope was determined at baseline using phenylephrine and sodium nitroprusside infusions. The subjects underwent cold pressor testing before and during beta-blockade. The R-R interval increased from 861+/-119 ms at baseline to 952+/-141 ms during beta-blockade (P<0.01). Blood pressure was 117+/-9/65+/-8 mm Hg at baseline and 117+/-10/67+/-8 mm Hg during beta-Blockade (P=NS). beta-Blockade did not affect baroreflex sensitivity (BRSup: 21+/-10 versus 28+/-11 ms/mmHg, P<0.1; BRSdown: 17+/-8 versus 20+/-8 ms/mmHg, P=NS). Muscle sympathetic nerve activity increased significantly during beta-blockade (number of bursts/100 beats: 32+/-9 versus 40+/-14, P<0.05), compared with baseline. However, the operating points of the parasympathetic and sympathetic baroreflex during beta-blockade were on the baroreflex curves obtained at baseline. beta-Blockade blunted the heart rate response to cold pressor testing; blood pressure and muscle sympathetic nerve activity responses were similar. Our study demonstrates that propranolol does not cause an acute decrease in sympathetic activity in normotensive young subjects. This, observation is not consistent with an important tonic stimulatory effect of beta-adrenoreceptors in the brain

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Stewart JM (2002). Pooling in chronic orthostatic intolerance: arterial vasoconstrictive but not venous compliance defects. Circulation.105:2274-2281.

Abstract: BACKGROUND: Orthostatic intolerance is characterized by postural tachycardia syndrome (POTS) with exaggerated tachycardia, orthostatic symptoms, and "pooling" (which comprises acrocyanosis and dependent edema when upright). My colleagues and I tested the hypothesis that pooling results from increased venous compliance in POTS patients. METHODS AND RESULTS: Fifteen patients aged 13 to 19 years were compared with 11 healthy, age-matched controls. The POTS group was divided into patients with high venous pressure (P(v)>20 mm Hg) and normal P(v) on the basis of resting supine P(v) obtained in previous work. Subjects were studied using strain gauge plethysmography to measure blood flow, P(v), and the venous compliance volume-pressure relation while supine and during incremental head-up tilt testing at -10 degrees, 0 degrees, 20 degrees, and 35 degrees. Volume-pressure relations of controls and POTS patients with normal P(v) and high P(v) were not different and were unchanged by orthostasis. Supine leg peripheral resistance was greater than control resistance in patients with high P(v) (54+/-9 versus 30+/-6 mm Hg x mL(-1) x 100 mL(-1) x min(-1)) and less than control resistance in patients with normal P(v) (17+/-2 mm Hg x mL(-1) x 100 mL(-1) x min(-1)). On upright tilt, resistance decreased in high P(v) to approximate resistance in normal P(v). Resistance in controls increased throughout tilt. Leg P(v) increased in patients with normal P(v) and in controls but remained unchanged in the high P(v) group. CONCLUSIONS: The findings suggest that pooling in POTS is due to blunted arterial vasoconstriction, which produces passive redistribution of blood within peripheral venous capacitance beds. Venous compliance in POTS is similar to that in control subjects

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O'Donovan D, Feinle C, Tonkin A, Horowitz M, Jones KL (2002). Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects. Journal of Physiology-London.540:673-679.

Abstract: Postprandial hypotension occurs frequently in older people and may lead to syncope and falls. Some recent studies suggest that the magnitude of the postprandial fall in blood pressure (BP) is influenced by the rate of gastric emptying. The aim of this study was, therefore, to determine whether the fall in blood pressure induced by intraduodenal glucose is influenced by the rate of nutrient delivery into the small intestine, bypassing the effects of gastric emptying. Eight healthy elderly subjects (four male and four female, age 70.3 +/- 3.4 years) were studied on two separate days, in double-blind, randomised order. Glucose was infused intraduodenally at a rate of either 1 or 3 kcal min(-1), for 60 min, (0-60 min) followed by 0.9 % saline for a further 60 min (60-120 min). Blood pressure and heart rate were recorded at baseline and every 3 min during the study. Blood glucose and plasma insulin were also determined. Only the 3 kcal min(-1) infusion caused a significant fall in systolic (P < 0.001) and diastolic (P < 0.0001) blood pressure and an increase in the heart rate (P < 0.0001). The rises in blood glucose (P < 0.01) and plasma insulin (P < 0.05) concentrations were greater during the 3 kcal min(-1) infusion. We conclude that in healthy older subjects, the magnitude of the fall in blood pressure and increase in heart rate induced by intraduodenal glucose infusion is dependent on the rate of nutrient delivery into the small intestine. These results may have relevance to the treatment of postprandial hypotension

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Shannon JR, Diedrich A, Biaggioni I et al (2002). Water drinking as a treatment for orthostatic syndromes. [see comments.]. American Journal of Medicine.112:355-360.

Abstract: PURPOSE: Water drinking increases blood pressure in a substantial proportion of patients who have severe orthostatic hypotension due to autonomic failure. We tested the hypothesis that water drinking can be used as a practical treatment for patients with orthostatic and postprandial hypotension, as well as those with orthostatic tachycardia. SUBJECTS AND METHODS: We studied the effect of drinking water on seated and standing blood pressure and heart rate in 11 patients who had severe orthostatic hypotension due to autonomic failure and in 9 patients who had orthostatic tachycardia due to idiopathic orthostatic intolerance. We also tested the effect of water drinking on postprandial hypotension in 7 patients who had autonomic failure. Patients drank 480 mL of tap water at room temperature in less than 5 minutes. RESULTS: In patients with autonomic failure, mean (+/- SD) blood pressure after 1 minute of standing was 83 +/- 6/53 +/- 3.4 mm Hg at baseline, which increased to 114 +/- 30/66 +/- 18 mm Hg (P <0.01) 35 minutes after drinking. After a meal, blood pressure decreased by 43 +/- 36/20 +/- 13 mm Hg without water drinking, compared with 22 +/- 10/12 +/- 5 mm Hg with drinking (P <0.001). In patients with idiopathic orthostatic intolerance, water drinking attenuated orthostatic tachycardia (123 +/- 23 beats per minute) at baseline to 108 +/- 21 beats per minute after water drinking ( P <0.001). CONCLUSION: Water drinking elicits a rapid pressor response in patients with autonomic failure and can be used to treat orthostatic and postprandial hypotension. Water drinking moderately reduces orthostatic tachycardia in patients with idiopathic orthostatic intolerance. Thus, water drinking may serve as an adjunctive treatment in patients with impaired orthostatic tolerance 

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