Figure 6.
Figure 6. Mechanism for thromboprotection in BKB2R-/- mice. This figure shows that in the absence of the BKB2R-/- receptor, plasma prekallikrein, bradykinin 1-5, and angiotensin II are elevated. Angiotensin II interacts with an overexpressed AT2R receptor to liberate increased NO and prostacyclin. The increased production of these endothelial-cell products lengthens the animals' bleeding time and lengthens the time to thrombosis on the Rose Bengal model for carotid artery thrombosis. HK indicates high-molecular-weight kininogen; PRCP, prolylcarboxypeptidase; AT1R, angiotensin AT1 receptor; AT2R, angiotensin AT2 receptor; NO, nitric oxide; PGI2, prostaglandin I2 or prostacyclin.

Mechanism for thromboprotection in BKB2R-/- mice. This figure shows that in the absence of the BKB2R-/- receptor, plasma prekallikrein, bradykinin 1-5, and angiotensin II are elevated. Angiotensin II interacts with an overexpressed AT2R receptor to liberate increased NO and prostacyclin. The increased production of these endothelial-cell products lengthens the animals' bleeding time and lengthens the time to thrombosis on the Rose Bengal model for carotid artery thrombosis. HK indicates high-molecular-weight kininogen; PRCP, prolylcarboxypeptidase; AT1R, angiotensin AT1 receptor; AT2R, angiotensin AT2 receptor; NO, nitric oxide; PGI2, prostaglandin I2 or prostacyclin.

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