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1 Franz Volhard Clinic and Max Delbruck Center for Molecular Medicine, Charite University Hosptial, Humboldt University of Berlin, HELIOS Klinikum Berlin, Berlin, Germany
* To whom correspondence should be addressed. E-mail: gollasch{at}fvk-berlin.de.
Blood vessels are surrounded by variable amounts of adipose tissue. We showed earlier that adventitial adipose tissue inhibits rat aortic contraction by release of a transferable factor (ADRF) that activates smooth muscle K+ channels. However, little is known about the mechanisms of ADRF release. Using isolated rat aortic rings and isometric contraction measurements, we show that ADRF release depends on extracellular [Ca2+] (EC50 ~ 4.7 mM). ADRF effects do not involve neuronal presynaptic N-type Ca2+ and Na+ channels or vanilloid, cannabinoid, and calcitonin gene-related peptide receptors. ADRF release is strongly inhibited by the protein tyrosine kinase inhibitors genistein and tyrphostin A25 (AG82). In contrast daidzein, an inactive genistein analog, and the protein tyrosine kinase inhibitor ST638 had no effect. Protein kinase A inhibition by H89 also inhibited ADRF release while the protein kinase G inhibitor KT5823 had no effect. We propose that ADRF release is Ca2+-dependent and is regulated by intracellular signaling pathways involving tyrosine kinase and protein kinase A. Furthermore, ADRF release does not depend upon perivascular nerve endings.
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