Vascular wall renin-angiotensin pathway in control of the circulation. A hypothesis.

Multiple lines of evidence support the existence of a vascular renin-angiotensin system independent of the circulating system. Vascular renin appears to originate from both uptake of plasma renin and in situ synthesis. Renin may bind to vascular endothelium. In addition, the endothelium is capable of activating inactive renin. Cell-surface-bound renin and angiotensin-converting enzyme constitute a biochemical cascade on the endothelial surface, resulting in a high local concentration of angiotensin. The role of the intracellular system is unclear. Intracellular angiotensin may regulate the angiotensin receptor and modulate the vascular response to exogenous angiotensins. Recent data also suggest that neutrophils and platelets provide mobile pathways by which cell-bound or released enzymes can activate and amplify the renin-angiotensin biochemical cascade. The mobile angiotensin pathways may be important in the inflammatory vascular response, edema formation, and vasospasm of vascular injury. Taken together, the vascular wall renin-angiotensin system may play an important role in cardiovascular homeostasis. We postulate that abnormalities in the control of this system may result in local vasospasm or systemic hypertension.