Clinical Pharmacology of Digitalis Glycosides

Doherty, JamesE.; Kane, James J.

doi:10.1146/annurev.me.26.020175.001111

Cited by 49 publications

(22 citation statements)

References 39 publications

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“…This is in agreement with the results obtained by Doherty [74]. However, the patients studied by Ohnhaus It is known that the impairment of renal function decreases digoxin clearance since the elimination of digoxin is correlated to creatinine clearance [74]. Thus, when cardiac failure is severe enough to impair renal function, a reductin in digoxin clearance is expected, leading to a longer half-life and increased plasma concentrations with possible toxicity.…”

Section: Digoxinsupporting

confidence: 90%

Effects of cardiovascular disease on pharmacokinetics

Rodighiero

1989

Cardiovasc Drug Ther

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The pathophysiologic changes occurring in cardiovascular disease can affect the kinetics of drugs in several different ways. The present review examines these modifications and the underlying mechanisms. The kinetics of specific agents, such as antiarrhythmic, antihypertensive, cardiotonic, and other drugs are considered, and the clinical implications are outlined. The clinician should be aware of these modifications, because they require an adjustment of the dosage regimen. A rational basis for a correct therapeutic choice can be provided by adequate knowledge of these modifications.

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Section: Digoxinsupporting

confidence: 90%

Effects of cardiovascular disease on pharmacokinetics

Rodighiero

1989

Cardiovasc Drug Ther

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“…63 As administration of excessive doses of digoxin leads to serious arrhythmias, the circulating levels of immunoreactive digoxin are monitored during digoxin therapy. Even when digoxin has not been given to patients, digoxin-like immunoreactivity (DLI) is sometimes detected in the plasma, 64, 65 possibly due to an EDLF that cross-reacts with the anti-digoxin antibody.…”

Section: The Role Of Endogenous Digitalis In Hypertensionmentioning

confidence: 99%

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

et al. 2011

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The central nervous system has a key role in regulating the circulatory system by modulating the sympathetic and parasympathetic nervous systems, pituitary hormone release, and the baroreceptor reflex. Digoxin- and ouabain-like immunoreactive materials were found >20 years ago in the hypothalamic nuclei. These factors appeared to localize to the paraventricular and supraoptic nuclei and the nerve fibers at the circumventricular organs and supposed to affect electrolyte balance and blood pressure. The turnover rate of these materials increases with increasing sodium intake. As intracerebroventricular injection of ouabain increases blood pressure via sympathetic activation, an endogenous digitalis-like factor (EDLF) was thought to regulate cardiovascular system-related functions in the brain, particularly after sodium loading. Experiments conducted mainly in rats revealed that the mechanism of action of ouabain in the brain involves sodium ions, epithelial sodium channels (ENaCs) and the renin–angiotensin–aldosterone system (RAAS), all of which are affected by sodium loading. Rats fed a high-sodium diet develop elevated sodium levels in their cerebrospinal fluid, which activates ENaCs. Activated ENaCs and/or increased intracellular sodium in neurons activate the RAAS; this releases EDLF in the brain, activating the sympathetic nervous system. The RAAS promotes oxidative stress in the brain, further activating the RAAS and augmenting sympathetic outflow. Angiotensin II and aldosterone of peripheral origin act in the brain to activate this cascade, increasing sympathetic outflow and leading to hypertension. Thus, the brain Na+–ENaC–RAAS–EDLF axis activates sympathetic outflow and has a crucial role in essential and secondary hypertension. This report provides an overview of the central mechanism underlying hypertension and discusses the use of antihypertensive agents.

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“…Hyperkalaemia is an important feature of severe digoxin poisoning and the initial serum potassium levels are related to the mortality (Bismuth et al, 1973;Smith and Willerson, 1971;Doherty, 1968). The hyperkalaemia is thought to be due to failure of the ATPase membrane pump and consequent leakage of potassium from the myocardial cells (Glynn, 1964).…”

Section: Discussionmentioning

confidence: 99%