Hypertension is characterized by an increased risk of thrombotic complications. This reviews describes the possible roles of tissue factor in the increased risk of thrombosis in hypertensive patients. Tissue factor is an integral membrane protein that represents the physiologic initiator of blood coagulation; its roles in thrombosis are also well documented. Activation of the renin angiotensin system may modulate tissue factor expression as shown by the stimulation brought about by Angiotensin II in human monocytes and smooth muscle cells, and in rat aortic endothelial cells and the inhibition obtained by renin angiotensin system blockade through angiotensin converting enzyme blockers, angiotensin type II receptor antagonists and direct renin inhibitors. Finally, in clinical trials, administration of angiotensin type 1 receptor antagonists to hypertensive patients reduced circulating tissue factor. P-selectin, an adhesion receptor expressed by activated platelets and endothelial cells, upregulates tissue factor synthesis by human monocytes. Since platelet activation accompanies hypertension, induction of tissue factor synthesis mediated, perhaps, by P-selectin may represent a further link between hypertension and thrombosis. Pharmacological interventions that reduce TF upregulation might contribute to reduce the risk of cardiovascular complications in these patients.
Tissue factor and systemic hypertension
CELI, ALESSANDRO;PEDRINELLI, ROBERTO
2010-01-01
Abstract
Hypertension is characterized by an increased risk of thrombotic complications. This reviews describes the possible roles of tissue factor in the increased risk of thrombosis in hypertensive patients. Tissue factor is an integral membrane protein that represents the physiologic initiator of blood coagulation; its roles in thrombosis are also well documented. Activation of the renin angiotensin system may modulate tissue factor expression as shown by the stimulation brought about by Angiotensin II in human monocytes and smooth muscle cells, and in rat aortic endothelial cells and the inhibition obtained by renin angiotensin system blockade through angiotensin converting enzyme blockers, angiotensin type II receptor antagonists and direct renin inhibitors. Finally, in clinical trials, administration of angiotensin type 1 receptor antagonists to hypertensive patients reduced circulating tissue factor. P-selectin, an adhesion receptor expressed by activated platelets and endothelial cells, upregulates tissue factor synthesis by human monocytes. Since platelet activation accompanies hypertension, induction of tissue factor synthesis mediated, perhaps, by P-selectin may represent a further link between hypertension and thrombosis. Pharmacological interventions that reduce TF upregulation might contribute to reduce the risk of cardiovascular complications in these patients.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
