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• Hypertensive response of water ingestion in chronic autonomic failure: refining underlying mechanism
  Vinod K Gupta
  Published on: 7 January 2005

• Published on: 7 January 2005

  Hypertensive response of water ingestion in chronic autonomic failure: refining underlying mechanism

  • Vinod K Gupta, Physician

  Dear Editor,

  Young and Mathias studied the cardiovascular effects of rapid water ingestion in multiple system atrophy (MSA) and pure autonomic failure (PAF) and discuss the possible mechanisms responsible for the hypertensive response. [1] Involvement of increased sympathetic nerve activity or denervation supersensitivity appears unlikely. Besides the response being as great in PAF as in MSA (with a more rapid ons...

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  Dear Editor,

  Young and Mathias studied the cardiovascular effects of rapid water ingestion in multiple system atrophy (MSA) and pure autonomic failure (PAF) and discuss the possible mechanisms responsible for the hypertensive response. [1] Involvement of increased sympathetic nerve activity or denervation supersensitivity appears unlikely. Besides the response being as great in PAF as in MSA (with a more rapid onset in PAF) and the greater probability of an increase in baseline blood pressure, [1] absence of tachycardia following water ingestion does not support the occurrence of sympathetic hyperfunction, either reactive or following denervation supersensitivity.

  Furthermore, measurement of muscle sympathetic nerve activity has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction that is unaccompanied by significant changes in arterial blood pressure. [2] Even in normal subjects, therefore, the relationship between water ingestion-related sympathetic activation and blood pressure is not straightforward. Finally, water drinking elicits a pressor response even if the direct connection between brain stem cardiovascular centers and spinal sympathetic neurons is interrupted. [3]

  While there is no known link between endothelin and water ingestion, the second suggested mechanism [1], vasopressin is suppressed following water ingestion. Vasopressin release cannot be targeted as a possible mechanism for the hypertensive response of water ingestion in MSA or PAF. To consider a state-related significant disruption of vasopressin secretion in the absence of a polyuric syndrome also challenges scientific logic; five minutes after water ingestion, when the pressor effect of water was first recorded [1], under normal circumstances hardly any water would have been absorbed to affect fluid or electrolyte balance. To suggest that rate of gastric water absorption might be different in MSA or PAF, an underlying gastric mechanistic link to the known pathophysiology of these conditions must be explicated to sustain the proposal. Finally, cholinergic neurons that regulate vasopressin release are damaged in MSA; metoclopramide that increases vasopressin in control subjects, does not increase vasopressin secretion in MSA patients. [4]

  Adaptation is a highly complex phenomenon. The body perceives the remote as well as the near, the future as well as the present. [5] Anticipatory reflexes possibly play an important homeostatic function in human physiology; vomiting is one example of such a mechanism. [6] The sympathetic nervous system regulates the renin-angiotensin system in the upright posture. The body might anticipate a water load as a threat to its integrity, particularly in the face of sympathetic nervous system impairment.

  Transiently improved renal perfusion following water ingestion might assist in handling the water load. Also, the renin-angiotensin system can raise the peripheral vascular resistance without causing tachycardia, as has been recorded in this study. This hypothesis can be investigated by studying release of renin following water ingestion in patients with chronic autonomic failure.

  As a management option for orthostatic symptoms, water drinking [1] is a rather inconvenient strategy that appears to have a temporally- limited hypertensive effect. Repeated water drinking during awake periods can be a demanding therapeutic manœuvre. Long-acting analogues of vasopressin or angiotensin II might manage symptomatic orthostatic hypotension much better. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume and has been proposed for the management of syncope. [7] Unlike rapid water drinking, with controlled administration of desmopressin the body is unlikely to perceive gradual fluid retention as a threat.

  References

  (1). Young TM, Mathias CJ. The effects of water ingestion on orthostatic hypotension in two groups of chronic autonomic failure: multiple system atrophy and pure autonomic failure. J Neurol Neurosurg Psychiatry 2004;75:1737-1741.

  (2). Scott EM, Greenwood JP, Gilbey SG, Stoker JB, Mary DA. Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects. Clin Sci (Lond) 2001;100:335-342.

  (3). Tank J, Schroeder C, Stoffels M, Diedrich A, Sharma AM, Luft FC, Jordan J. Pressor effect of water drinking in tetraplegic patients may be a spinal reflex. Hypertension 2003;41:1234-1239.

  (4). Norbiato G, Bevilacqua M, Righini V, Chebat E, Vago T, Bertora P, Castelli L, Mangoni A. Altered vasopressin response to metoclopramide in multiple system atrophy: evidence of a cholinergic defect in the hypothalamus. Acta Neurol Scand 1992;85:299-303.

  (5). Carell A. Man, the unknown. Hamish Hamilton Ltd., London. 1959, p.149.

  (6). Gupta VK. Cyclic vomiting syndrome: anticipatory stress response in migraine? Headache 2003;44:106-107.

  (7). Hilz MJ, Marthol H, Neundorfer B. Syncope - a systematic overview of classification, pathogenesis, diagnosis and management. Fortschr Neurol Psychiatr 2002;70:95-107.

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  Conflict of Interest:
  None declared.

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