Evaluation of the secretory pattern of plasma arginine vasopressin in stroke patients.
ABSTRACT Arginine vasopressin (AVP) may play a role in the development of ischemic brain edema and/or cerebral vasospasm. Data available on AVP plasma levels in ischemic stroke are few and discordant. In order to ascertain whether changes in AVP plasma levels occur in ischemic stroke, plasma AVP levels, plasma osmolality and mean arterial pressure were determined in 24 patients with unprecedented ischemic cerebral infarction and in 15 controls over a 24-hour period. In stroke patients, mean 24-hour plasma AVP levels (7.2 +/- 0.8 ng/l) were higher (p < 0.05) than in control subjects (2.4 +/- 0.3 ng/l), and correlated with the severity score of the neurologic deficit and the mean size of the lesion. In patients with a more severe neurologic deficit, the mean 24-hour plasma AVP levels (8.7 +/- 1.0 ng/l) were higher than in patients with a less severe neurologic deficit (5.2 +/- 0.8 ng/l). Data indicate that in ischemic stroke an increased AVP secretion occurs independently of osmotic or baroreceptorial mechanisms. The possibility that AVP may play a role in neuronal cell damage following cerebral ischemia warrants further attention.
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ABSTRACT: It is well known that vasopressin participates in the regulation of the cardiovascular system, water electrolyte balance and many functions of the central nervous system. Receptors for vasopressin are widely distributed throughout the brain. They are present in neurons, in astrocytes and their perivascular processes, in endothelial and smooth muscle cells of blood vessels and in choroid plexus. Such a location suggests that vasopressin may participate in the regulation of vascular resistance in cerebral circulation and water homeostasis in the brain. Present review of the data published on this subject suggests that endogenous vasopressin is involved in brain pathology rather than in physiological regulations. Numerous studies have shown increased release of vasopressin and expression of vasopressin receptors in the brain following ischemia, trauma or subarachnoid hemorrhage in patients and in animal models of these diseases. Moreover, it has been demonstrated that antagonists of vasopressin V(1a) receptors are able to alleviate brain edema and spastic changes in blood vessels after subarachnoid hemorrhage. Vasopressin is also implicated in brain edema and in impairment of cerebral vasculature in hypo-osmotic states. The discussed results suggest that vasopressin V(1a) receptors antagonists may be a useful tool for the treatment of some states associated with cerebrovascular pathology.Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 01/2009; 59 Suppl 8:109-16. · 2.27 Impact Factor