Effects of nonspecific β-adrenergic stimulation and blockade on blood coagulation in hypertension
| Autor: | Paul J. Mills, Elaine Dillon, Roland von Känel, Karen A. Adler, Joel E. Dimsdale, Christy J. Perez |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Adult
Male Sympathetic nervous system medicine.medical_specialty Physiology Adrenergic beta-Antagonists Stimulation Fibrin Fibrinogen Degradation Products Double-Blind Method Von Willebrand factor Physiology (medical) Internal medicine von Willebrand Factor Humans Medicine Hemostatic function Blood Coagulation Cross-Over Studies Dose-Response Relationship Drug biology business.industry Isoproterenol Adrenergic beta-Agonists Middle Aged Propranolol Blockade Autonomic nervous system medicine.anatomical_structure Endocrinology Coagulation Hemostasis Hypertension biology.protein Female business |
| Zdroj: | Journal of Applied Physiology. 94:1455-1459 |
| ISSN: | 1522-1601 8750-7587 |
| DOI: | 10.1152/japplphysiol.00892.2002 |
| Popis: | 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 nonspecific β-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−1 · min−1 for 15 min/dose. Thirteen subjects were double-blind studied after receiving placebo or propranolol (100 mg/day) for 5 days each. In hypertensive subjects, isoproterenol elicited a dose-dependent increase in plasma von Willebrand factor (vWF) antigen [ F(2,34) = 5.02; P = 0.032] and a decrease in D-dimer [ F(2,34) = 4.57; P = 0.040], whereas soluble tissue factor remained unchanged. Propranolol completely abolished the increase in vWF elicited by isoproterenol [ F(1,12) = 10.25; P = 0.008] but had no significant effect on tissue factor and D-dimer. In hypertension, vWF is readily released from endothelial cells by β-adrenergic stimulation, which might contribute to increased cardiovascular risk. However, β-adrenergic stimulation alone may not be sufficient to trigger fibrin formation in vivo. |
| Databáze: | OpenAIRE |
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