Specific role of tyrosine kinase in the vascular contraction produced by stretch.

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In order to determine whether protein tyrosine kinase mechanisms are involved in pressure-induced contraction, we compared effects of three structurally-unrelated tyrosine kinase inhibitors and orthovanadate, a tyrosine phosphatase inhibitor, on the pressure-induced contraction of the posterior cerebral artery isolated from rats. The change in vessel diameter was continuously measured with a width analyzer. Herbimycin A inhibited the pressure-induced contraction, while it only slightly inhibited contractions produced by potassium chloride or 9,11 dideoxy-11alpha, 9alpha-epoxymethano prostaglandin F2alpha (U46619). Genistein inhibited not only the pressure-induced contraction but also the U46619-induced one. Tyrphostin 23 significantly attenuated contractions in response to three different stimuli, i.e., pressure, potassium chloride, and U46619. Orthovanadate potentiated the pressure-induced contraction. These results suggest that herbimycin A is the most specific and potent inhibitor of the pressure-induced contraction and that a protein tyrosine kinase machanism may play an important role in the genesis of the pressure-induced contraction of the rat cerebral artery.