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Drugs in pregnancy and lactation
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
All components of the renin-angiotensin system (RAS) exist within the fetal kidney during the early stages of development and participate as promoting factors for the growth of this organ, more specifically its angiogenesis, and have an important role in controlling intrarenal haemodynamics [25–27]. In the early fetal stage, renin-containing cells are present in the developing intrarenal branches of the renal artery. Renin is also distributed in other vascular parts including the arcuate, interlobar and afferent arterioles. Renin mRNA gene expression markedly increases throughout fetal life to peak in the perinatal period. This gene could be under the influence of adrenergic input, as its expression is abolished with renal denervation [26]. In early life, renin is almost exclusively detected in the juxtaglomerular apparatus. Renin acts on plasma angiotensinogen to form angiotensin I.
Inherited Susceptibility to Metabolic Complications of Obesity
Published in Claude Bouchard, The Genetics of Obesity, 2020
Roger R. Williams, Paul N. Hopkins, Steven C. Hunt, M. Catherine Schumacher, Barry M. Stults, Lily L. Wu, Sandra J. Hasstedt
As a second genetic category, multiple discrete susceptibility genes cause predispositions that are strongly dependent on other factors for expression. Examples would include urinary kallikrein excretion, which shows strong major gene effects and seems to offer a liability for hypertension, but not predominant determination.26 Low potassium intake is an important environmental cofactor for renal kallikrein. Another recently determined gene from molecular studies is the angiotensinogen locus, which seems to promote moderately severe blood pressure elevation in about 5% of persons with hypertension.27 Again, by itself this gene probably does not cause hypertension.27 Many common disorders probably require two or three of these common genetic mechanisms to produce a strong genetic predisposition. Thus, hypertension or lipid abnormalities that are common usually reflect the combined effects of one or two of these multiple discrete genes in addition to other factors such as age and environment.
Renal, Cardiovascular, and Pulmonary Functions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Renin enzymatically converts circulating angiotensinogen, made by the liver, into angiotensin I. The inactive angiotensin I is then converted into active angiotensin II by angiotensin-converting enzyme (ACE). ACE is produced in the lungs but binds to the surface of endothelial cells in the afferent arterioles and the glomerulus. Angiotensin II acts systemically as a potent vasoconstrictor, and it also causes constriction of both the afferent and efferent arterioles of the glomerulus. In cases of blood loss or dehydration, angiotensin II reduces both glomerular filtration rate (GFR), and renal blood flow, thus limiting fluid loss and preserving blood volume. The release of angiotensin II is stimulated by decreases in blood pressure, underlying its primary role in the preservation of adequate blood pressure.
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).
Association between endothelial nitric oxide synthase and the renin-angiotensin-aldosterone system polymorphisms, blood pressure and training status in normotensive/pre-hypertension and hypertensive older adults: a pilot study
Published in Clinical and Experimental Hypertension, 2021
Roberta Fernanda da Silva, Riccardo Lacchini, Lucas Cezar Pinheiro, Letícia Perticarrara Ferezin, José Eduardo Tanus-Santos, Marcelo Rizzatti Luizon, Thiago José Dionísio, Carlos Ferreira Santos, Thaís Amanda Reia, André Mourão Jacomini, Ana Maria Guilmo Moreno, Anderson Saranz Zago
Conversely, the study by Agachan et al. (46), conducted in Turkey with 194 participants, sought to define an association between angiotensin AT1 receptor A1166C polymorphism and HA. As a result, the authors found that TT genotype of the angiotensinogen M235T polymorphism, D allele of the ACE I/D polymorphism and also AC + CC genotypes were more frequent in hypertensive than normotensive/pre-hypertension. Furthermore, (49)Pinheiro et a). indicated that the combination of the DD/G genotype of ACE and ACE 2 polymorphisms, respectively, may play a role in predisposition of SBP. This result suggested that the increased activity of ACE (pro-hypertensive effects) in combination with reduced ACE 2 activity (antihypertensive effects) could be the underlying mechanism. The association of ACE D allele with lipid alterations indicate that this result can be a marker of poor prognosis of SBP which contribute to CVD development.
Approach to Nutrition in Cancer Patients in the Context of the Coronavirus Disease 2019 (COVID-19) Pandemic: Perspectives
Published in Nutrition and Cancer, 2021
Adriana Garófolo, Lyon Qiao, Priscila dos Santos Maia-Lemos
Furthermore, there is evidence to suggest that vitamin D3 regulates the renin-angiotensin system by inhibiting renin and the ACE-Angiotensin II-AT1 receptor cascade. The renin-angiotensin system regulates blood pressure by converting angiotensinogen into angiotensin I and finally, into angiotensin II. The latter transformation is catalyzed by ACE2, a membrane peptidase. As the entry of SARS-CoV-2 into human cells is thought to occur via ACE2, vitamin D may play a role in the prevention of SARS-CoV-2 infection. Given this potential relationship, the vitamin D supplementation in normal or vitamin D-deficient individuals may serve an important role in boosting the immune system to fight COVID-19 infection, reducing COVID-19 severity, and preventing acute lung injury, especially in people with associated co-morbidities (63–65).