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Molecular Basis of Na, K-ATPase Regulation of Diseases: Hormone and FXYD2 Interactions.

Int J Mol Sci

December 2024

Instituto de Bioquímica Médica Leopoldo de Meis, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-590, RJ, Brazil.

The Na, K-ATPase generates an asymmetric ion gradient that supports multiple cellular functions, including the control of cellular volume, neuronal excitability, secondary ionic transport, and the movement of molecules like amino acids and glucose. The intracellular and extracellular levels of Na and K ions are the classical local regulators of the enzyme's activity. Additionally, the regulation of Na, K-ATPase is a complex process that occurs at multiple levels, encompassing its total cellular content, subcellular distribution, and intrinsic activity.

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Background: This study examines genetic variations in the systemic oxygen transport cascade during exhaustive exercise in physically trained tactical athletes. Research goal: To update the information on the distribution of influence of eleven polymorphisms in ten genes, namely ACE (rs1799752), AGT (rs699), MCT1 (rs1049434), HIF1A (rs11549465), COMT (rs4680), CKM (rs8111989), TNC (rs2104772), PTK2 (rs7460 and rs7843014), ACTN3 (rs1815739), and MSTN (rs1805086)-on the connected steps of oxygen transport during aerobic muscle work.

Methods: 251 young, healthy tactical athletes (including 12 females) with a systematic physical training history underwent exercise tests, including standardized endurance running with a 12.

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Background: Patients with severe respiratory failure have high mortality and need various interventions. However, the impact of intensivists on treatment choices, patient outcomes, and optimal intensivist staffing patterns is unknown. In this study, we aimed to evaluate treatments and clinical outcomes for patients at board-certified intensive care training facilities compared with those at non-certified facilities.

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Decreased urinary excretion of norepinephrine and dopamine in autonomic synucleinopathies.

Clin Auton Res

December 2024

Autonomic Medicine Section (AMS), Clinical Neurosciences Program (CNP), Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), 10 Center Drive MSC-1620, Building 10 Room 8N260, Bethesda, MD, 20892-1620, USA.

Article Synopsis
  • Autonomic synucleinopathies like Parkinson's disease (PD), pure autonomic failure (PAF), and multiple system atrophy (MSA) are characterized by autonomic failure and the abnormal buildup of alpha-synuclein protein in the body. !* -
  • Research showed that patients with these conditions had significantly lower urinary excretion rates of norepinephrine and dopamine compared to controls, suggesting a potential dysfunction in their renal sympathetic function. !* -
  • The study analyzed urine samples from participants at the NIH over nearly three decades and found no significant differences in DOPA and epinephrine levels among the groups, indicating that only norepinephrine and dopamine were impacted by these diseases. !*
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Article Synopsis
  • Acute kidney injury (AKI) often occurs in patients with vasodilatory shock and is linked to higher mortality rates, longer hospital stays, and potential chronic kidney disease.
  • A comparison of catecholamine vasopressors (like norepinephrine and epinephrine) with non-catecholamine options (like vasopressin and angiotensin II) indicated that catecholamines could worsen kidney function and recovery.
  • Research showed that non-catecholamine vasopressors were associated with better renal outcomes, including lower serum creatinine levels and reduced need for kidney replacement therapy.
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