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J Appl Physiol (December 13, 2002). doi:10.1152/japplphysiol.00892.2002
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Articles in PresS, published online ahead of print December 13, 2002
J Appl Physiol, 10.1152/jap.00892.2002
Submitted on September 26, 2002
Accepted on December 3, 2002

EFFECTS OF NON-SPECIFIC {beta}-ADRENERGIC STIMULATION AND BLOCKADE ON BLOOD COAGULATION IN HYPERTENSION

Roland von Kanel1, Joel E Dimsdale2, Karen A Adler2, Elaine Dillon2, Christy J Perez2, and Paul J Mills2*

1 Department of Psychiatry, University of California San Diego, La Jolla, CA, USA; Institute for Behavioral Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland
2 Department of Psychiatry, University of California San Diego, La Jolla, CA, USA

* To whom correspondence should be addressed. E-mail: pmills{at}ucsd.edu.

A hypercoagulable state might contribute to increased atherothrombotic risk in hypertension. The sympathetic nervous system is hyperactive in hypertension, and it regulates hemostatic function. We investigated the effect of non-specific {beta}-adrenergic stimulation (isoproterenol) and blockade (propranolol) on clotting diathesis in hypertension. Fifteen hypertensive and 21 normotensive subjects underwent isoproterenol infusion in two sequential fixed-order doses of 20 and then 40 ng/kg/min for 15 min/dose. Double-blind, 13 subjects were studied once receiving placebo and once receiving propranolol (100 mg/d) for 5 days each. In hypertensive subjects, isoproterenol elicited a dose-dependent increase in plasma von Willebrand factor (vWF) antigen (F2,34= 5.02, p=.032), and a decrease in D-dimer (F2,34= 4.57, p=.040), whereas soluble tissue factor (TF) remained unchanged. Propranolol completely abolished the increase in vWF elicited by isoproterenol (F1,12= 10.25, p=.008) but had no significant effect on TF and on D-dimer. In hypertension, vWF is readily released from endothelial cells by {beta}-adrenergic stimulation, which might contribute to increased cardiovascular risk. However, {beta}-adrenergic stimulation alone may not be sufficient to trigger fibrin formation in vivo.







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