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Am J Physiol Heart Circ Physiol. 2003 Jul;285(1):H305-15. Epub 2003 Mar 20.
Calcium dynamics in the failing heart: restoration by beta-adrenergic receptor blockade.

Plank DM, Yatani A, Ritsu H, Witt S, Glascock B, Lalli MJ, Periasamy M, Fiset C, Benkusky N, Valdivia HH, Sussman MA.

Divisions of Molecular Cardiovascular Biology, The Children's Hospital and Research Foundation, Cincinnati, OH 45229, USA.

Changes in calcium (Ca2+) regulation contribute to loss of contractile function in dilated cardiomyopathy. Clinical treatment using beta-adrenergic receptor antagonists (beta-blockers) slows deterioration of cardiac function in end-stage heart failure patients; however, the effects of beta-blocker treatment on Ca2+ dynamics in the failing heart are unknown. To address this issue, tropomodulin-overexpressing transgenic (TOT) mice, which suffer from dilated cardiomyopathy, were treated with a nonselective beta-receptor blocker (5 mg. kg-1. day-1 propranolol) for 2 wk. Ca2+ dynamics in isolated cardiomyocytes of TOT mice significantly improved after treatment compared with untreated TOT mice. Frequency-dependent diastolic and Ca2+ transient amplitudes were returned to normal in propranolol-treated TOT mice and but not in untreated TOT mice. Ca2+ kinetic measurements of time to peak and time decay of the caffeine-induced Ca2+ transient to 50% relaxation were also normalized. Immunoblot analysis of untreated TOT heart samples showed a 3.6-fold reduction of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), whereas Na+/Ca2+ exchanger (NCX) concentrations were increased 2.6-fold relative to nontransgenic samples. Propranolol treatment of TOT mice reversed the alterations in SERCA and NCX protein levels but not potassium channels. Although restoration of Ca2+ dynamics occurred within 2 wk of beta-blockade treatment, evidence of functional improvement in cardiac contractility assessed by echocardiography took 10 wk to materialize. These results demonstrate that beta-adrenergic blockade restores Ca2+ dynamics and normalizes expression of Ca2+-handling proteins, eventually leading to improved hemodynamic function in cardiomyopathic hearts.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12649072&dopt=Abstract

Alcohol. 2000 Aug;22(1):53-6.
Augmentation of corticosterone release by means of a caffeine-ethanol interaction in rats.

Kunin D, Gaskin S, Rogan F, Smith BR, Amit Z.

Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, 1455 de Maisonneuve Boulevard, West, H-1013, H3G 1M8, Montreal, Quebec, Canada. kunisbn.concordia.ca

We examined whether the acute treatment with caffeine delivered before an ethanol injection would augment plasma corticosterone (CORT) levels. The effect of caffeine on blood ethanol levels was also assessed. After 10 days of acclimatization to the colony room conditions, male Wistar rats were injected with either caffeine (5 mg/kg, ip) or saline 30 min before the delivery of ethanol (0.8 g/kg, ip) or saline, respectively. Trunk blood was then collected at 15 and 30 min after the ethanol injection for determination of plasma CORT and blood ethanol levels. CORT was measured with the use of radioimmunoassay, and blood ethanol levels were determined with the use of gas chromatography. The results showed that although caffeine and ethanol delivered singly failed to augment plasma CORT levels, the combination of both drugs produced elevations in plasma CORT levels at 15 and 30 min. These findings were found to be unrelated to changes in ethanol metabolism as caffeine failed to alter blood ethanol levels within the period tested. It was argued that the present elevations in plasma CORT levels observed in animals administered caffeine and ethanol may play a role in the caffeine-induced elevations in ethanol drinking observed elsewhere.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11109028&dopt=Abstract

Auton Neurosci. 2000 Oct 30;84(1-2):30-9.
Differential distribution of ionic channels and muscarinic receptors at the cat tracheal neuromuscular junction.

Tanaka K, Inoue R, Ikarashi Y, Maruyama Y, Sugimachi K, Ito Y.

Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

The ionic and pharmacological properties of atropine-sensitive excitatory junction potentials (EJPs) were investigated by the double sucrose gap and microelectrode membrane potential recording methods, and compared with those of inward currents evoked by carbachol (I(CCh)), in cat tracheal smooth muscle. A single and repetitive field stimulation (10-30 V, 50 micros, 20 Hz) evoked atropine-inhibitable EJPs and associated twitch-like contractions. Reduction in external Na+ concentration strongly, but in the external Cl- concentration, decreased the EJP amplitude after 5 min superfusion, although prolonged exposure to low Cl- solutions attenuated the EJPs modestly. Chloride channel blockers such as 9-AC and niflumic acid (each 100 microM), at concentrations high enough to inhibit I(CCh) almost completely, failed to abolish the EJPs. Pirenzepine, AF-DX116 and 4-DAMP all effectively inhibited the EJPs at their concentrations to block respective muscarinic receptor subtypes relatively specifically, while depletion of internal stores by 10 mM caffeine and/or 3 microM ryanodine caused only a partial decrease in the EJP amplitude. These properties are considerably different from those of I(CCh) which is activated exclusively through activation of the M3 receptor/IP3-mediated Ca2+ release pathway and reflects mostly a Ca2+-dependent Cl- current, and suggests the differential distribution of muscarinic receptors and ionic channels inside and outside of the cholinergic neuromuscular junction of this muscle.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11109987&dopt=Abstract

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