Abstract
The renin-angiotensin system regulates blood pressure, and maintains electrolyte homeostasis in humans [1]. In this system, angiotensinogen (AGT) is catalyzed by renin to form angiotensin I, which is then cleaved by angiotensin-converting enzyme (ACE) to yield angiotensin II, a potent vasopressor and effector on renal function [1]. Recently, several studies have focused on the correlation between physiological disorders and the genetic variation of peptides in the reninangiotensin system. A specific mutation in the angiotensinogen gene was reported to be associated with essential hypertension [2,3]. Individuals with homozygous deletion alleles of ACE were reported to have a higher level of serum ACE and an increased risk of ischemic heart disease, sudden death, left ventricular hypertrophy, increased blood glucose levels, diabetic nephropathy, and premature death [4–7]. Detection of mutations in genes that constitute the renin-angiotensin system may be important in the prevention and control of disorders in the cardiovascular system, glucose metabolism, and urinary function.
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© 2001 Springer-Verlag Berlin Heidelberg
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Sakai, E., Tajima, M., Mori, M., Inage, R., Fukumoto, M., Nakagawara, KI. (2001). Genotyping of Angiotensin-Converting Enzyme and Angiotensinogen Polymorphisms with the LightCycler System. In: Meuer, S., Wittwer, C., Nakagawara, KI. (eds) Rapid Cycle Real-Time PCR. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59524-0_16
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DOI: https://doi.org/10.1007/978-3-642-59524-0_16
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