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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Treatment is with ACE inhibitors, angiotensin receptor antagonists or beta blockers to block the renin cycle (beta blockers reduce renin output from the juxtaglomerular apparatus). Diuretics promote sodium excretion. Hypertensive encephalopathy, pulmonary oedema or severe acute disease may require IV treatment with sodium nitroprusside, hydralazine, labetalol or a nitrate preparation. IV sodium nitroprusside therapy allows minute-by-minute blood pressure control, but toxic cyanide metabolites can accumulate. If renal artery stenosis is present, a sudden reduction in blood pressure can reduce renal perfusion and worsen renal function.
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, 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.
Prediction of pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
The biggest group of tests studied are biochemical tests. Some of the biochemical tests are also used in prognostication of the disease. A classic example of this is serum uric acid level estimation. All the chemical substances studied are from diverse families, including hormones, proteins, enzymes, receptors and the like. The list seems to be unending. Estimation of complex biochemical substances never became popular because their efficacy and clinical application remained limited. A classic example of this is the estimation of renin-angiotensin sensitivity test.
Serum uric acid: a futile bystander in endothelial function?
Published in Blood Pressure, 2023
Benjamin De Becker, Philippe Van De Borne
The estimated glomerular filtration rate was calculated using the CKD-EPI Creatinine Equation [19]. Oxidative stress was assessed using the ratios of homocitrulline/lysine and 3-chlorotyrosine/tyrosine, as well as the concentration of allantoin. 3-chlorotyrosine is a specific oxidation product of tyrosine by oxidants, and oxidants may catalyse the formation of homocitrulline from lysine. The measurement of homocitrulline/lysine and 3-chlorotyrosine/tyrosine involved acid hydrolysis, derivatization, and liquid chromatography-mass spectrometry tandem (LC-MS/MS) [20]. Allantoin, which indicates oxygen free radical load and is the result of a nonenzymatic reaction between UA and reactive oxygen species (ROS), was measured using LC-MS/MS. Angiotensin II levels were measured using an ELISA kit.
Valsartan-mediated chronotherapy in spontaneously hypertensive rats via targeting clock gene expression in vascular smooth muscle cells
Published in Archives of Physiology and Biochemistry, 2022
Jiajie Luan, Kui Yang, Yanyun Ding, Xiaotong Zhang, Yaqin Wang, Haiju Cui, Deixi Zhou, Lu Chen, Zhangqing Ma, Wusan Wang, Wen Zhang, Xiaoyun Liu
Angiotensin II (ANG II), belonging to the renin-angiotensin-aldosterone system, is an endogenous vasoconstrictor that elevates BP. ANG II binds to angiotensin type 1 (AT1) receptors, which induces activation of downstream signalling pathways to trigger phosphorylation of 20-kDa regulatory myosin light chain (MLC20); this represents a primary mechanism for regulating smooth-muscle contractions, which ultimately induces vascular smooth muscle contractions to raise BP. Valsartan is a competitive AT1 receptor antagonist that inhibits the endogenous effects of ANG II to lower BP. It has been demonstrated that valsartan yields significantly different efficacies between awake time and asleep time administrations. However, whether valsartan targets central and/or peripheral circadian clocks to modulate circadian BP remains unknown. Moreover, although clock genes control circadian BP rhythms, whether these clock-gene rhythms are altered under disease conditions also remains largely unknown.
Cabergoline versus calcium infusion in the prevention of ovarian hyperstimulation syndrome: a randomised controlled study
Published in Journal of Obstetrics and Gynaecology, 2022
Usama M. Fouda, Hesham S. Elshaer, Gamal G. Youssef, Amal Hanafy, Waleed M. Mehrem, Mohamed A. Youssef, Mona Farouk, Hala Nabil
Renin is an enzyme which catalyses the conversion of angiotensinogen produced by the liver to angiotensin I. Angiotensin-converting enzyme (ACE) on the surface of vascular endothelial cells converts angiotensin I to angiotensin II. Renin is the rate limiting step of the activity of RAS system because the half life of angiotensin II is less than one minute and the angiotensinogen production by the liver is almost constant (Palumbo et al. 2016). The role of calcium in the regulation of renin secretion has been proposed. In vivo and in vitro studies revealed that renin secretion is inversely related to the extracellular and intracellular calcium concentrations. Calcium influences renin secretion through modification of synthesis and degradation of cAMP which is the dominant stimulatory secondary messenger of renin secretion. Increased intracellular calcium decreases the activity of adenylyl cyclase-V (the enzyme that catalyses the conversion of ATP to cAMP) therefore decreases the formation of cAMP and the release of renin (Beierwaltes 2010).