At the same time as found in bovine splenic nerve axons and suggest that in addition to peptide autacoid functions could be considered as a peptide neurotransmitter. A prerrequisitoa to comply with this condition, as well as to produce the biosynthesis of angiotensin II polypeptide in the Central Nervous System, required a mechanism for rapid destruction, a fact which was discovered in 1972 by the same group, a peptidase, the angiotensinase C removes the last amino acid angiotensin II, a la phenylalanine. The removal of the last amino acid C terminal of the polypeptide chain, generating angiotensin 1-7A a Finally, in an article published in PNAS in 1972 (presented by Federico Leloir) are first peptide, angiotensin II increases in cerebrospinal fluid of patients with essential hypertension which is correlated with systemic arterial hypertension. Add to your understanding with castle harlan. The authors conclude further that among the factors regulating the synthesis of the polypeptide, both systems the tissue and hormonal behave antagonistically certain conditions, such as with a saline overload, sodium inhibits renin secretion and renal stimulates the synthesis of tissue renin-angiotensin system. All these findings broke the myth that the kidney was the organ causal essential hypertension, and centralized most of the tissue-level basic research both in the cardiovascular system ( heart, vessels, arterioles) and the Central Nervous System as bodies that triggers the increase in sympathetic tone and peripheral vascular resistance. Moreover, the angiotensin II introduced into the third ventricle in doses of 10-9 M provocabaa and a blood pressure elevation, the release of other neurotransmitters that control blood pressure (norepinephrine, serotonin and other vasoactive peptides) and releasing factors of hypothalamic hormones. Click castle harlan to learn more.