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Placental Nutrient Metabolism and Transport
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
The mechanisms by which the amino acids are actively transported by placental tissues are under investigation (Table 4). At least for system A, cotransport occurs with inwardly directed Na+ transport that is energized by Na+/K+-ATPase producing an outside/inside Na+ electrochemical gradient. System L appears regulated by H+-amino acid cotransport that involves H+ out per Na+ + amino acid in, also energized by Na+/K+-ATPase.100, 101 These transport mechanisms are active at the maternal brush-border but also may be responsible for transport on the fetal side. Studies of dually (maternal and fetal side) perfused placentas with paired tracers of amino acids indicate bidirectional transport for many amino acids but with different transport kinetics such that transplacental transfer is greater in the maternal-fetal direction for all of the amino acids taken up the placenta.84 This net flux is largely accounted for by a faster placental-to-fetal efflux compared to placental-to-matemal efflux, rather than to different rates of uptake between the maternal and fetal surfaces. The mechanisms that account for the directionality of transplacental transfer are still under investigation.
Antihypertensive Drug Classes
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Engi Abdel-Hady Algharably, Reinhold Kreutz
Thiazide and thiazide-like diuretics are commonly grouped together and referred to as thiazide diuretics (3). These agents promote natriuresis and diuresis depleting body stores of sodium which results in lowering of BP. They act primarily by inhibiting the Na+/Cl- cotransporter in the distal tubule of the kidney, which inhibits Na+ reabsorption (1). Because this transporter only reabsorbs a small fraction (about 5%) of filtered Na+, thiazides are less potent than loop diuretics. The latter act proximally at the ascending limb of the loop of Henle (3). The effects of thiazide diuretics on BP is triphasic: (i) short term, (ii) long term, and (iii) chronic. In the short-term phase (i.e. first 2–4 weeks), reductions in BP occur due to the decrease in plasma volume which reduces cardiac output. A countereffect elicited by consecutive rise in plasma renin and transient increase in peripheral vascular resistance opposes the BP-lowering effect. During the long-term phase, BP is still lowered due to a gradual reduction in peripheral vascular resistance, while cardiac output and plasma volume return to pretreatment levels. A chronic antihypertensive effect is reached after about 2 months due to a persistent reduction in peripheral resistance, where a new steady state of reduced total body sodium and BP is established (2).
The [Na+,K+,Cl−] Cotransport System: Relevance in Essential Hypertension
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
Ricardo P. Garay, Sylvie Cavalier, Patrick A. Hannaert
The [Na+,K+,Cl−]-cotransport system is a membrane transport protein which exists in almost every cell in which it has been investigated.5-7 The cotransport system is perhaps the most complex ion transport protein because under physiological conditions it moves six translocating substrates; i.e., it catalyzes coupled fluxes of sodium, potassium, and chloride in both inward and outward directions across the cell membrane (Figure 1).
Efficacy and safety of finerenone for treatment of diabetic kidney disease: current knowledge and future perspective
Published in Expert Opinion on Drug Safety, 2022
Vincenzo Marzolla, Marco Infante, Andrea Armani, Manfredi Rizzo, Massimiliano Caprio
Sodium–glucose cotransporter-2 inhibitors (SGLT2is) are a relatively novel class of drug for treating T2DM that are recommended in T2DM patients with established cardiorenal disease, including T2DM patients with CKD [92]. Indeed, SGLT2is have been shown to significantly reduce cardiorenal events in patients with T2DM [93]. Sodium–glucose cotransporter-2 (SGLT2) is mainly localized in the proximal convoluted renal tubule, and mediates glucose reabsorption by the kidney. Inhibition of this cotransporter determines the excretion of glucose and sodium in the urine, reducing blood glucose levels, promoting osmotic diuresis, and favoring blood pressure reduction [94]. Finerenone exerts its renal protective effects in patients with T2DM and CKD by preserving eGFR, reducing inflammation, fibrosis, and albuminuria, while SGLT2i exert their renal protective effects through eGFR preservation, reduction of blood pressure and tubular/glomerular damage, improvement in albuminuria, and reduction of ischemic renal damage by promoting autophagy and mitochondrial biogenesis [95,96]. This point appears to be particularly important in the absence of evidence regarding whether the combination therapy, using a SGLT2i and finerenone, could lead to greater cardiorenal benefits than SGLT2i or finerenone monotherapies in patients with T2DM and CKD.
Specific FSTL1 polymorphism may determine the risk of cardiomyopathy in patients with acromegaly
Published in Acta Cardiologica, 2022
Suleyman Nahit Sendur, Tuncay Hazirolan, Busra Aydin, Incilay Lay, Mehmet Alikasifoglu, Tomris Erbas
The study was designed as a cross-sectional case research. The study was approved by the institutional noninterventional clinical research ethics board with the project no: GO 17/898 and was performed in accordance with the ethical standards of the Helsinki Declaration and its later amendments. Informed consent was obtained from all individual participants included in the study. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Forty-six consecutive acromegalic patients were included in the study. The patients who had a history of past cardiac surgery; any cardiac diseases that may affect heart morphology such as congenital heart diseases, valvular diseases, pulmonary hypertension, cardiac tumours; past medical history of myocarditis and any contraindication for MR imaging were excluded. The patients who had chronic kidney disease, congestive heart failure and/or chronic liver disease were excluded as well. Subjects that receiving thyroid hormone, gonadal steroid and/or glucocorticoid replacement were required to receive stable doses for at least last three months to include the study. None of the subjects with diabetes mellitus were on sodium-glucose cotransporter-2 inhibitor treatment.
The cytokine storm of COVID-19: a spotlight on prevention and protection
Published in Expert Opinion on Therapeutic Targets, 2020
Lucie Pearce, Sean M. Davidson, Derek M. Yellon
In other cardioprotective developments, research is ongoing to identify the exact mechanisms by which sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial in the diabetic heart [73]. Treatments targeting ischemia induced microvascular dysfunction may equally be of interest in COVID-19. In addition to P2Y12 inhibitors and statins, Rho Kinase inhibitors (ROCKi) have demonstrated many novel actions in cardiovascular protection, including modulation of vascular tone, angiogenesis and apoptosis [70, 75, 76]. ROCK inhibition can additionally mediate endothelial barrier function and reduce leukocyte migration [77, 78]. These protective effects have been seen in the CNS in addition to the cardiovascular system [77], which makes this class of drug a versatile and exciting prospect for further research.