Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain its effects by causing increased vasodilation and decreased blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. Third, ATII increases blood pressure through direct arterial vasoconstriction. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. First, it stimulates the secretion of aldosterone from the adrenal cortex.
ATII increases blood pressure using a number of mechanisms. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. This promotes vasodilation and BP reduction.Ĭaprine, an ACE inhibitor, antagonizes the effect of the RAAS. Reduction of ATII leads to decreased Na and water retention. It also increases plasma renin activity and bradykinin levels. Caprine competitively inhibits the conversion of angiotensin I (ATI) to angiotensin II (ATII), thus resulting in reduced ATII levels and aldosterone secretion.
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