Cardiovascular Risk Factors
Nicole M. Farmer, Andres Victor Ardisson Korat in Cooking for Health and Disease Prevention, 2022
RAAS is an essential part of blood pressure regulation. The system consists of enzymes and chemical messengers and involves multiple organs. The first step in RAAS is the liver’s production of angiotensinogen, which is converted by the enzyme renin into angiotensin I. This is the rate-limiting step in the RAAS system. Angiotensin I is then converted mostly in the lungs into angiotensin II by ACE. Angiotensin II has biological effects on blood pressure, including constriction of blood vessels, sodium and water retention by kidneys, and atherosclerotic changes to the vessels. The actions from angiotensin II stimulate the production of aldosterone in the adrenal glands. Aldosterone in turn also has blood pressure-related effects as it increases sodium and water retention by the kidneys. In addition to functioning at a multiorgan level, the RAAS system can also function at local organ levels, such as blood vessels and the heart.
Miscellaneous Neuropeptides
Paul V. Malven in Mammalian Neuroendocrinology, 2019
Angiotensin II. This compound functions as both a blood-borne hormone and a CNS-produced neuropeptide (Phillips, 1987). Within the CNS, angiotensin II is widely distributed, but it is especially concentrated within and adjacent to circumventricular organs. The peripheral actions of angiotensin II include stimulating the release of aldosterone from the adrenal gland and raising blood pressure. In the CNS, angiotensin II acts upon the subfornical organ discussed in Chapter 4 to stimulate drinking behavior. Angiotensin II is also present in LH-containing cells of the adenohypophysis, and CNS angiotensin II may also influence the release of LHRH. There is also evidence that CNS angiotensin II may modulate other hypophysiotrophic neurohormones to influence the release of PRL and ACTH (Ganong, 1989).
Practice Paper 6: Answers
Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar in Get ahead! Medicine, 2016
Renal artery stenosis is typically seen in patients with atherosclerotic disease or fibromuscular dysplasia. The arterial stenosis results in renal hypoperfusion, which in turn stimulates the secretion of renin from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen into angiotensin. Angiotensin is converted to angiotensin II by angiotensin-converting enzyme (ACE). In patients with renal artery stenosis, angiotensin II is responsible for maintaining the glomerular filtration pressure by constricting the efferent arterioles in the nephron. If patients with bilateral renal stenosis are prescribed ACE inhibitors such as ramipril, the reduced synthesis of angiotensin II means that the efferent arterioles can no longer constrict, which results in loss of glomerular filtration pressure and the development of acute renal failure. For this reason, ACE inhibitors and angiotensin II receptor blockers are contraindicated in patients with known renal artery stenosis.
The effects of cardiac drugs on human erythrocyte carbonic anhydrase I and II isozymes
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Onur Argan, Kübra Çıkrıkçı, Aybike Baltacı, Nahit Gencer
Captopril is a competitive inhibitor of angiotensin converting enzyme (ACE). This enzyme is responsible for the conversion of angiotensin I to angiotensin II. Angiotensin II regulates blood pressure and is a key element of the renin–angiotensin–aldosterone system. Leppala et al. reported that captopril is an angiotensin I converting enzyme inhibitor with an IC50 value of 0.007 µM33. ACE inhibitors improve endothelial function, retard the progression of atherosclerosis, and reduce the risk of cardiovascular death, myocardial infarction, and stroke via ventricular remodelling and neurohumoral regulation. Therefore, these agents are recommended in the treatment of a wide range of diseases, including coronary artery disease, peripheral artery disease, heart failure, stroke, diabetes, and hypertension34. CA inhibition by captopril may be an additional pathway to prevent atherosclerosis.
Protective effects of combined Losartan and Nilotinib on carbon tetrachloride (CCl4)-induced liver fibrosis in rats
Published in Drug and Chemical Toxicology, 2020
Jamshid Karimi, Adel Mohammadalipour, Nasrin Sheikh, Iraj Khodadadi, Mohammad Hashemnia, Farjam Goudarzi, Vahid Khanjarsim, Ghasem Solgi, Mehrdad Hajilooi, Majid Bahabadi, Nejat Kheiripour, Keshvad Hedayatyanfard
Ang II is a peptide hormone that raises blood pressure by binding to its own receptor, especially receptor type I angiotensin II (AT1-R). This receptor is highly active in patients with the chronic liver disease, such as cirrhosis (Salama et al. 2016). It has been shown that activation of HSCs increases the expression of TGF-β1 and collagen-1 gene by AngII (Marshall et al. 2000). In other words, similar myofibroblast cells that are activated from HSCs are inhibited by an ANGII blocker with the help of the AT1R antagonist or angiotensin-converting enzyme inhibitor (ACEI) (Kim et al. 2008, Salama et al. 2016). The strong anti-fibrotic effect of the AT1R blocking compounds is also noted in relation to ACEIs. Therefore, Losartan, an AT1 receptor antagonist, has shown a novel effect in inhibiting the progression of liver fibrosis, which was performed by inhibiting TGF-β (Salama et al. 2016). Co-administration of both Imatinib and Losartan have been reported to have a stronger effect rather than the administration of each compound alone (Yoshiji et al. 2006). Hence, due to the stronger effect of Nilotinib compared with Imatinib in inhibiting fibrosis, we assume that the inhibition of combined AT1R (losartan) and TKIs (Nilotinib) may have a dramatic effect on the onset and progression of liver fibrosis.
Autophagy contributes to angiotensin II induced dysfunction of HUVECs
Published in Clinical and Experimental Hypertension, 2021
Di Liu, Wan-Pin Sun, Jing-Wei Chen, Yan Jiang, Rong Xue, Lin-Hui Wang, Koji Murao, Guo-Xing Zhang
Angiotensin II (Ang II) is one of the main components of the renin-angiotensin-aldosterone system and plays an important role in maintaining plasma sodium concentration, arterial blood pressure and extracellular volume. Over-secretion of Ang II results in an overwhelming number of chronic and acute diseases, such as hypertension, cell proliferation, inflammation, and fibrosis (1–3). Increasing number of investigation demonstrates the crucial role of Ang II in the development of cardiovascular diseases (4,5). Our previous studies have revealed that Ang II activates NADPH oxidase to increase the production of reactive oxygen species (ROS), leading to mitochondria release large amount of ROS, resulting in activation downstream signaling pathways (6,7), which subsequently has been confirmed by other investigators (8–10). Up to date, ROS has been demonstrated as one of the key regulators in mediating Ang II–induced tissue damage (11,12). Antioxidant therapy is now being supposed to as a supplement method in clinical patients with high Ang II level.
Related Knowledge Centers
- Adrenal Cortex
- Blood Pressure
- Peptide
- Peptide Hormone
- Liver
- Vasoconstriction
- Renin–Angiotensin System
- Aldosterone
- Hormone
- Dipsogen