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ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction).
Angiotensin III increases blood pressure and stimulates aldosterone secretion from the adrenal cortex; it has 100% adrenocortical stimulating activity and 40% vasopressor activity of angiotensin II. Angiotensin IV also has adrenocortical and vasopressor activities. Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to ...
Contrastly, TXA 2 vascular tissue synthesis is stimulated by angiotensin II which promotes cyclooxygenase I's metabolism of arachidonic acid. An angiotensin II dependent pathway also induces hypertension and interacts with TXA 2 receptors.
Angiotensin I is then almost immediately converted by an enzyme already present in the blood to the active form of the protein, angiotensin II. Angiotensin II then travels in the blood until it reaches the posterior pituitary gland and the adrenal cortex, where it causes a cascade effect of hormones that cause the kidneys to retain water and ...
The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to G q/11 and G i/o and thus activates phospholipase C and increases the cytosolic Ca 2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C.
However, when the blood circulates through the lungs a pulmonary capillary endothelial enzyme called angiotensin-converting enzyme (ACE) cleaves a further two amino acids from angiotensin I to form an octapeptide known as angiotensin II. Angiotensin II is a hormone which acts on the adrenal cortex, causing the release into the blood of the ...
In the opposite case, juxtaglomerular cells are stimulated to release more renin, which stimulates the renin–angiotensin system, producing angiotensin I which is converted by Angio-Tensin Converting Enzyme (ACE) to angiotensin II. Angiotensin II then causes preferential constriction of the efferent arteriole of the glomerulus and increases ...
It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide. It is very efficient, since more than 25,000 m mol /day of sodium is filtered into the nephron , but only ~100 mmol/day, or less than 0.4% remains in the final urine.