<unk>  activates the<unk> –angiotensin system by using it's endopeptidase activity to cleave angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin–converting enzyme primarily within the capillaries of the lungs. Angiotensin II then constricts blood vessels, increases the secretion of ADH and aldosterone, and stimulates the hypothalamus to activate the thirst reflex, each leading to an increase in blood pressure.<unk> 's primary function is therefore to eventually cause an increase in blood pressure, leading to restoration of perfusion pressure in the kidneys.<unk>  is secreted from juxtaglomerular kidney cells, which sense changes in<unk> al perfusion pressure, via stretch receptors in the vascular walls. The juxtaglomerular cells are also stimulated to release<unk>  by signaling from the macula densa. The macula densa senses changes in sodium delivery to the distal tubule, and responds to a drop in tubular sodium load by stimulating<unk>  release in the juxtaglomerular cells. Together, the macula densa and juxtaglomerular cells comprise the juxtaglomerular complex.<unk>  secretion is also stimulated by sympathetic nervous stimulation, mainly through β1 adrenoreceptor activation. The (pro)renin receptor to which<unk>  and prorenin bind is encoded by the gene ATP6ap2, ATPase H(+)-transporting lysosomal accessory protein 2, which results in a fourfold increase in the conversion of angiotensinogen to angiotensin I over that shown by soluble<unk>  as well as non-hydrolytic activation of prorenin via a conformational change in prorenin which exposes the catalytic site to angiotensinogen substrate. In addition,<unk>  and prorenin binding results in phosphorylation of serine and tyrosine residues of ATP6AP2. The level of<unk>  mRNA appears to be modulated by the binding of HADHB, HuR and CP1 to a regulatory region in the 3' UTR.
Renin
Prorenin
Adrenalone
Thyroglobulin
Prolene
Modulin
Orexin
Vasopressin