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Influence of medication on typical exercise response
Published in R. C. Richard Davison, Paul M. Smith, James Hopker, Michael J. Price, Florentina Hettinga, Garry Tew, Lindsay Bottoms, Sport and Exercise Physiology Testing Guidelines: Volume II – Exercise and Clinical Testing, 2022
Most angiotensin-converting-enzyme (ACE) inhibitors attenuate the activity of angiotensin-converting enzyme, an important component of the renin-angiotensin system, which can exist as both a membrane-bound and a circulating enzyme. High levels of membrane-bound ACE exist in skeletal muscle. Inhibition of this enzyme prevents the formation of Angiotensin II, which is a potent vasoconstrictor, and it hydrolyses Bradykinin, which is a vasodilator. This synergistic combination of actions drops the blood pressure through reduced peripheral resistance (Byrd et al., 2019). Interestingly, ACE-1 also decreases centrally driven thirst mechanisms (Dundas et al., 2007) and prevents erythropoiesis (Cruzado et al., 2008). Acute bouts of exercise increase the production of ACE (Magalhães, 2020). Depending on the dosage of the medication, this could lead to profound blood-pressure-lowering effects of ACE, leaving an individual with feelings of light-headedness, nausea or even fainting. Ways to counter this are to check resting blood pressure before exercise and increase the load gradually in order to mitigate this risk. Conversely, chronic exercise exposure leads to lower circulating levels of ACE, which may mean that, in poorly controlled hypertensives, the effect of the medication is diminished (Klöting, 2020).
Genetic Limitations to Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
ACE is part of the renin–angiotensin system and is involved in blood pressure regulation and fluid–electrolyte balance. This gene contains a common (∼40% minor allele frequency; MAF) well-studied 287-bp Alu insertion/deletion polymorphism in intron 16 (Ensembl Variant rs1799752). The insertion (I) allele is associated with lower levels of circulating (68) and tissue (33) ACE activity, whilst the deletion (D) allele is associated with higher levels of circulating and tissue ACE activity (61). The ACE enzyme is a dipeptidase catalysing the conversion of inactive angiotensin I to active angiotensin II. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide. Consequently, the ACE I/D polymorphism has the potential to alter blood pressure control and fluid electrolyte balance, depending on which version of the gene individuals carry. Control of blood flow to working muscles and fluid–electrolyte balance is crucial for sporting activity, making ACE I/D an excellent candidate polymorphism for sporting performance.
Regulation of Arterial Blood Pressure
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
The renin–angiotensin system is the most important renal–body fluid mechanism and, therefore, long-term blood pressure control. A decrease in arterial blood pressure causes a decrease in renal perfusion which is sensed by mechanoreceptors in the afferent arterioles of the kidneys. This results in renin secretion by the juxtaglomerular cells. Renin catalyses the conversion of angiotensinogen to angiotensin I in plasma. In the lungs and kidneys, angiotensin I is converted to angiotensin II. Angiotensin II activates G-protein-coupled angiotensin receptors (AT1) in adrenal cortex, vascular smooth muscle, kidneys and brain. Angiotensin II acts on the zona glomerulosa of the adrenal cortex to synthesize and secrete aldosterone. Aldosterone acts on the principal cells of the collecting duct to increase absorption and thereby increase blood and extracellular fluid (ECF) volume. Angiotensin II also stimulates the Na+/H+ exchanger in the proximal tubule of the kidneys and increases the reabsorption of Na+ and HCO3−. Angiotensin II also acts on the hypothalamus to increase thirst and water intake and stimulates ADH release, which increases water reabsorption in the collecting ducts. Angiotensin II binds to G-protein-coupled receptors on arterioles and activate the IP3/Ca++ second messenger system to cause vasoconstriction. The resulting increase in total peripheral resistance leads to an increase in arterial blood pressure.
Crescents proportions above 10% are associated with unfavorable kidney outcomes in IgA nephropathy patients with partial crescent formation
Published in Renal Failure, 2023
Dingxin Di, Lin Liu, Ying Wang, Yue Yang, Shimin Jiang, Wenge Li
The use of renin-angiotensin system (RAS) inhibitors, including angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 receptor blockers (ARBs), was recorded. In addition, data on the use of immunosuppressive medications, including a full dose of oral prednisone (starting from 0.8–1 mg/kg per day and regularly reduced) in conjunction with or without glucocorticoid pulse therapy (e.g., intravenous methylprednisolone 500 mg for 1 to 3 times), and immunosuppressants (including cyclophosphamide, mycophenolate mofetil, leflunomide, and cyclosporine), were also collected. The kidney endpoint was a composite of ≥40% decline in the initial eGFR [14], end-stage kidney disease (ESKD), and death due to kidney disease. ESKD was defined as the initiation of kidney replacement therapy including maintenance dialysis or kidney transplantation. Survival time was defined as the interval from the time of kidney biopsy to one of the three endpoints: kidney endpoint, loss to follow-up, or the study end date (September 2022).
Antioxidant-rich Terminalia catappa fruit exerts antihypertensive effect via modulation of angiotensin-1-converting enzyme activity and H2S/NO/cGMP signalling pathway in Wistar rats
Published in Biomarkers, 2023
Adeniyi A. Adebayo, Ayokunle O. Ademosun, Bukola C. Adedayo, Ganiyu Oboh
One of the strategies for the control of high blood pressure is the inhibition of angiotensin-1-converting enzyme (ACE). Uncontrolled elevation of ACE activity produces angiotensin II, a potent vasoconstrictor, from angiotensin I (Akinyemi et al., 2015). Results in this study showed that Terminalia catappa fruits-supplemented diets attenuate ACE activity, further substantiate the effect on hemodynamic parameters earlier presented. The role of renin-angiotensin system in controlling blood pressure, fluid and electrolyte homeostasis, renal and vascular function, and myocardial remodelling is curtailed by ACE (Brewster et al., 2003, Akinyemi et al., 2015). Thus, its inhibition is paramount to high blood pressure management (Akinyemi et al., 2015). Previous studies have shown phenolics-ACE kinetics, where phenolic compounds such as caffeic, ellagic, gallic, and chlorogenic acids competitively inhibited ACE activity (Agunloye et al., 2019, Chen et al., 2023). Thus, the effect of Terminalia catappa fruits on ACE activity observed in this study could be partly linked to the inherent phenolic compounds.
Angiotensin II receptor blockers in dermatology: a narrative review
Published in Journal of Dermatological Treatment, 2022
Both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II (ATII) receptor blockers (ARBs) block the renin-angiotensin system (RAS) (1). They are the most commonly used antihypertensive agents (2). ARBs act against hypertension through the selective inhibition of ATII (2), which results in fewer adverse reactions than those engendered by ACEIs because the action does not affect bradykinin degradation (2). Both ACEIs and ARBs are first-line treatment options for hypertension, and there are no differences in cardiovascular outcomes (3), but patients usually tolerated better ARB, with fewer adverse effects, such as cough and angioedema. Furthermore, the adverse cutaneous effects engendered by ARB use are smaller than those by ACEIs and calcium channel blockers (CCBs) (4,5). However, there are fewer reports on the clinical applications of ARBs in dermatology than those of ACEIs (6) and CCBs (7). To address this knowledge gap in the literature, this review article presents up-to-date information on ARB use in dermatology and the corresponding cutaneous adverse reactions (Tables 1 and 2).