We examined the chronotropic and sympathoadrenal responses to a strenuous exercise in eight normal subjects receiving placebo and carteolol, a nonselective beta-adrenoceptor blocker. Plasma catecholamines were measured with high-performance liquid chromatography with electrochemical detection (HPLC-ECD). Mean plasma norepinephrine (NE) and epinephrine (E) concentrations attained at 0.5 and 2 min after exercise were significantly (p less than 0.001-0.05) greater in the carteolol trial than in the placebo trial and approached concentrations fairly similar to preexercise baseline values by 15 min after cessation of exercise in the two trials. The postexercise plasma NE and E concentration-chronotropic response relationships were shifted to the right in the carteolol as compared with the placebo phase. The maximal postexercise NE concentrations measured during the placebo trial correlated significantly with beta-adrenoceptor blockade (p less than 0.05, r = 0.74), whereas the relationship between E concentrations and beta-adrenoceptor blockade did not reach significant level in this small group of study subjects. The results suggest that beta-adrenoceptor blockade increases plasma concentrations of both NE and E during an earlier postexercise period and may cause a greater reflex sympathetic activation as compared with the adrenal response. However, the mechanism(s) remains unclear. Whether the exercise-induced NE rather than E would participate more predominantly in the chronotropic response to beta-adrenoceptor blockade requires further studies.
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Clin Toxicol (Phila)
January 2025
Clinical Toxicology Research Group, University of Newcastle, Newcastle, Australia.
Introduction: Propranolol is a beta-adrenoceptor blocking drug with sodium channel-blocking properties that can cause life-threatening toxicity in overdose. Limited research defines dose thresholds of toxicity. We aimed to investigate propranolol overdose and dose thresholds for severe toxicity.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University, 2-2-1 Miyama Funabashi, Chiba 274-8510, Japan.
The pulmonary vein wall contains a myocardial layer whose ectopic automaticity is the major cause of atrial fibrillation. This review summarizes the results obtained in isolated pulmonary vein myocardium from small experimental animals, focusing on the studies with the guinea pig. The diversity in the action potential waveform reflects the difference in the repolarizing potassium channel currents involved.
View Article and Find Full Text PDFClin Exp Pharmacol Physiol
October 2024
Department of Physiology, Federal University of Sergipe, Sao Cristovao, Brazil.
S-Limonene (s-Lim) is a monocyclic monoterpene found in a variety of plants and has been shown to present antioxidant and cardioprotective activity in experimental models of myocardial infarction. The aim of this study was to evaluate the potential mechanism by which s-Lim exerts its antiarrhythmic effect, focusing on the blockade of β-adrenoceptor (β-AR) and its effects on various in vivo and in vitro parameters, including electrocardiogram (ECG) measurements, left ventricular developed pressure (LVDP), the β-adrenergic pathway, sarcomeric shortening and L-type calcium current (I). In isolated hearts, 10 μM of s-Lim did not alter the ECG profile or LVPD.
View Article and Find Full Text PDFJ Pharmacol Sci
October 2024
Department of Pharmacology, Faculty of Medicine, Toho University, 5-21-16 Omori-nishi, Ota-ku, Tokyo, 143-8540, Japan. Electronic address:
J Mol Med (Berl)
October 2024
Sunnybrook Research Institute, Toronto, ON, Canada.
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