Renin-angiotensin-aldosterone system (RAAS) pathway and its function
Figure1. Renin-angiotensin-aldosterone system (RAAS) pathway (http://en.wikipedia.org/wiki/Renin-angiotensin_system)
When blood volume is low, the kidneys secreterenin. Renin stimulates the production of angiotensin. Angiotensin causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin also stimulates the secretion of the hormonealdosteronefrom the adrenal cortex. There are two types of Angiotensin (ⅠandⅡ ). Angiotensin Ⅰ is converted toangiotensin Ⅱ byangiotensin-converting enzyme(ACE) which is a key enzyme in RAAS, resulting in a strong contraction of blood vessels since angiotensin Ⅱ has a 10-40 times pressurization compared to epinephrine. Meanwhile, Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure. If RAAS is too active, blood pressure will be too high1,2
Studies showed that some key genes in RAAS, such as angiotensinogen (AGT) gene and angiotensin-converting enzyme (ACE) gene, are not only closely related to increased activity of RAAS, but also associated with hypertension, even other hypertension-related diseases. Furthermore, accumulating evidence suggests that genetic susceptibility to hypertension, as well as salt avidity and cardiovascular reactivity are ancestral and were likely magnified during the early human evolution prior to the out-of-Africa expansion of anatomically modern humans3-5. Subsequently, different susceptibilities to hypertension among human populations are due to disparate selection pressures during the out-of-Africa expansion 30,000 to 100,000 years age, and the most important selection pressure was climate which produced a latitudinal cline in hypertension susceptibility6.
References:
1.Ryan MJ, Sigmund CD: ACE, ACE inhibitors, and other JNK. Circ Res 2004; 94: 1-3.
2.Boron WF: Medical Physiology: A Cellular And Molecular Approaoch. Elsevier Saunders, 2003.
3.Baker EH, Ireson NJ, Carney C, Markandu ND, MacGregor GA: Transepithelial sodium absorption is increased in people of African origin. Hypertension 2001; 38: 76-80.
4.Vollmer WM, Sacks FM, Ard J et al: Effects of diet and sodium intake on blood pressure: Subgroup analysis of the DASH-sodium trial. Ann Intern Med 2001; 135: 1019-1028.
5.Sawka MN, Montain SJ, Latzka WA: Hydration effects on thermo-regulation and performance in the heat. Comp Biochem Physiol A MolIntegr Physiol 2001; 128: 679-690.
6.Young JH: Evolution of blood pressure regulation in humans. Curr Hypertens Rep 2007; 9: 13-18.