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The patient with acute renal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The kidney secretes an enzyme called renin from cells in the juxtaglomerulus apparatus, and this plays a significant role in regulating fluid balance and subsequently in controlling blood pressure. Renin is a vasoconstrictor and it leads to the release of other substances with similar properties. The chain of events that it initiates is collectively known as the renin–angiotensin–aldosterone system. Renin leads to the release of angiotensinogen, produced by hepatocytes, and converted in the plasma into angiotensin 1. This is then converted in the lungs into angiotensin 2, a very powerful vasopressor. The latter has two main functions: Vasoconstriction of the afferent arterioles, leading to a reduced glomerular filtration rate.Activation of aldosterone from the adrenal cortex, which leads to the reabsorption of sodium into the extracellular space, with chloride and water following it.
Mechanisms of Chemically Induced Glomerular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Glomerular dysfunctions observed in animal models of acute renal failure, where alterations of the renin-angiotensin system have been well documented, were produced after a short time interval following treatment.50–52 On the contrary, aminoglycoside-induced glomerular dysfunction is a rather late manifestation during the course of the toxicity in man and experimental animals.25,42 Another study on the renin-angiotensin system and gentamicin-induced nephrotoxicity by Luft et al.54 suggested that the elevated plasma renin activity could be an effect rather than a cause of the renal failure.
Applied Physiology: Renal Failure
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Major endocrine functions of the kidney include the control of red cell formation via erythropoietin synthesized in the peritubular cells and the control of arterial blood pressure via the renin–angiotensin system. Renal failure can lead to anaemia and hypertension. In early renal failure, renin is secreted from the juxtaglomerular cells in the ischaemic areas of the kidney. Renin activates the renin–angiotensin–aldosterone system. Angiotensin II causes vasoconstriction and stimulates the aldosterone (which increases Na+ and water retention) release from the adrenal cortex. This would account for hypertension in early renal failure.
Reduction of proteinuria in patients with diabetes kidney disease and dysautonomia through measures aimed at controlling supine hypertension
Published in Chronobiology International, 2022
Guilherme Palhares Aversa Santos, Douglas Inomata Cardoso da Silva, Vanessa Burgugi Banin, Silméia Garcia Zanati Bazan, Pasqual Barretti, Roberto Jorge da Silva Franco, Luis Cuadrado Martin
Seventeen patients were studied, eight in the historical control group and nine in the intervention group. The mean age of these patients was 64 ± 10 years, with a predominance of females in the control group and males in the intervention group. Follow-up time for patients was eleven months. Renin-angiotensin system inhibitors were used by all patients. Between groups, there was no statistical difference in the number of antihypertensive classes used by the patients (angiotensin converting enzyme inhibitors or angiotensin receptor blockers: 8 vs. 8, p = 1.00; diuretics: 7 vs. 7, p = 0.484; beta blockers: 4 vs. 4, p = 0.832; calcium channel blockers: 4 vs. 3, p = 0.258, respectively for intervention vs. control group). In the historical con-trol group, the mean time of diabetes diagnosis was 18 years, while in the intervention group, it was 22 years, with no statistical difference. Table 1 shows the demographic and clinical characteristics of the patients.
Mechanistic links between systemic hypertension and open angle glaucoma
Published in Clinical and Experimental Optometry, 2022
Ying-kun Cui, Li Pan, Tim Lam, Chun-yi Wen, Chi-wai Do
Third, the Renin-Angiotensin system may present a common pathway through which blood pressure and intraocular pressure are regulated. Renin-Angiotensin system plays an essential role in the pathophysiology of hypertension. It consists of dozens of angiotensin peptides, among which two axes of Renin-Angiotensin system cascades have been extensively studied, namely Angiotensin Converting Enzyme 1, Angiotensin II, and Angiotensin Type 1 Receptor axis (ACE1-Angiotensin II-ATR1) and Angiotensin Converting Enzyme 2, Angiotensin (1-7), and Mas Receptor axis (ACE2- Angiotensin (1-7)-Mas).52 Over-activation of ACE1-Angiotensin II-ATR1 is believed to be detrimental to the cardiovascular system and exacerbates hypertension, because it can induce vasoconstriction, increased secretion of aldosterone, and proliferation and increased collagen synthesis of vascular smooth muscle cells.53
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).