High blood pressure. Causes, symptoms, treatments

Lefunomide in combination therapy.

2017-05-06

Cardiac myocytes are continuously exposed to extracellular nucleotides secreted by the myocytes themselves, nerve terminals, or platelets and other blood cells during coronary perfusion, and the concentrations of such extracellular nucleotides are known to increase during cardiac ischemia and hypoxia. The effects of the extracellular nucleotides ATP, ADP, UTP, and adenosine on ventricular arrhythmogenic properties were explored in 36 Langendorff-perfused mouse hearts using monophasic action potential recording. Extracellular nucleotides induced arrhythmic phenomena in form of ectopic activity and ventricular tachycardia in a potency order of ATP (n=7) > ADP (n=5) > UTP (n=3) approximately adenosine (n=3). The purinergic receptor antagonists suramin and pyridoxal phosphate-6-azo(benzene-2,4-disulphonic acid) reduced the incidence of ATP-triggered arrhythmias. In isolated ventricular myocytes, ATP induced sustained increases in diastolic Ca2+ and triggered multiple Ca2+ waves, which were inhibited by suramin but not by the L-type Ca2+ channel antagonist nifedipine. In whole-cell patch clamp experiments, extracellular ATP induced two distinct types of inward currents, which were inhibited by suramin and PPADS, suggesting activation of P2X receptors. ATP also induced delayed after-depolarizations and ectopic action potentials in current clamped ventricular myocytes. In conclusion, extracellular ATP activates purinergic receptors and induces arrhythmic activity through modifications of Ca2+ homeostasis and an activation of depolarizing membrane currents.

This was a retrospective chart review of women who were admitted to BC Women's Hospital and Health Centre (1997-2001) and were given intravenous magnesium sulfate for preeclampsia. Serious magnesium-related effects were compared among 162 cases who received magnesium sulfate and contemporaneous nifedipine and 215 control subjects who received magnesium sulfate and either another antihypertensive (n=32 women) or no antihypertensive (n=183 women) medication. Chi-squared test, Fisher's exact test, or the Student t test was used for data comparison between cases and each control group. A probability value of <.05 was considered statistically significant.

The paper discusses the main approaches to slowing the progression and epy regression of atherosclerosis. Lipid and non-lipid treatment of atherosclerosis described. The results of clinical studies of the effect of antiatherosclerotic agents are analyzed. The main indicator is the thickness of the intima-media complex of the carotid arteries as measured by ultrasonography.

The lack of comparative studies of nifedipine and felodipine using 24-h blood pressure (BP) monitoring in the same patients led to the present study evaluating the antihypertensive efficacy and side effects of treatment with slow-release (SR) nifedipine (20 mg twice daily) and extended-release (ER) felodipine (10 mg once daily). In the double-blind study, subjects were randomly assigned to one of two treatment groups: 6 weeks of nifedipine SR (20 mg twice daily) followed by 6 weeks of felodipine (ER) (10 mg once daily with evening matched placebo), or vice versa. Twenty-four-hour ambulatory BP monitoring showed no significant differences in systolic BP (SBP) during the day. There were no significant differences in diastolic BP (DBP) throughout the 24 h, although the frequency of DBP recordings > 90 mm Hg was greater during nifedipine (33.1%) than felodipine (27.75%) treatment. The most common side effects were flushing, palpitations, headaches, and ankle edema; there were no adverse effect on lipid profile or glucose level.

Etomidate minimally influences hemodynamics at a standard induction dose in young healthy patients, but can cause significant systemic hypotension at higher doses for induction or electroencephalographic burst suppression (i.e., cerebral protection) in patients with advanced age or heart disease, and during cardiopulmonary bypass. However, less is known about its action on systemic resistance arteries.

The modulation of spontaneous release of acetylcholine by specific Ca2+ channel blockers was studied at neonatal rat neuromuscular junction. During early postnatal periods (0-4 days), blockers of N- and P/Q-type Ca2+ channels did not affect miniature endplate potential (MEPP) frequency. Unexpectedly, treatment with the L-type Ca2+ channel antagonist nifedipine, although not when treated with isradipine, nitrendipine, or calciseptine, resulted in strong increase in MEPP frequency. The potentiation effect of nifedipine was dose-dependent with a 56-fold maximum effect with 15 microM. The effect decreased during the first two postnatal weeks and disappeared by the third. The effect of nifedipine was not dependent on extracellular Ca2+ and was not altered by the presence of other Ca2+ channel blockers. In contrast, it was abolished by depleting intracellular Ca2+ stores with 2 microM thapsigargin and was partially inhibited by 10 microM ryanodine. In conclusion, we report a new ryanodine receptor-mediated effect of nifedipine on neonatal neuromuscular junction that may indicate the developmental expression of a specific receptor channel that interacts with intracellular Ca2+ stores. This effect of nifedipine should also be considered when using this drug as either a therapeutic or a research tool.