1 Adrenoceptor mediated decrease in pHi in quiescent ventricular myocardium
| Autor: | Mono Kanno, Shuzo Matsumoto, Haruaki Nakaya, Satoru Shida |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Male
medicine.medical_specialty Physiology Heart Ventricles Intracellular pH Adrenergic beta-Antagonists Guinea Pigs Stimulation Propranolol Membrane Potentials Amiloride Propanolamines Phenylephrine chemistry.chemical_compound Culture Techniques Physiology (medical) Internal medicine Isoprenaline medicine Animals Acidosis Forskolin Chemistry Myocardium Colforsin Isoproterenol Hydrogen-Ion Concentration Stimulation Chemical Endocrinology Atenolol DIDS Female Receptors Adrenergic beta-1 medicine.symptom Cardiology and Cardiovascular Medicine medicine.drug |
| Zdroj: | Cardiovascular Research. 28:112-118 |
| ISSN: | 0008-6363 |
| DOI: | 10.1093/cvr/28.1.112 |
| Popis: | Objective: The aims were to examine the effect of β adrenergic stimulation on the intracellular pH (pHi) and to compare it with that of α adrenergic stimulation in ventricular myocardium. Methods: Using conventional and ion selective electrodes membrane potential and pHi were measured simultaneously in quiescent papillary muscles of guinea pigs in HEPES or bicarbonate buffered solution. Isoprenaline and propranolol (1 μM) plus phenylephrine (30 μM) were used to stimulate β and α adrenoceptors, respectively. In order to evaluate underlying mechanism(s) of β adrenoceptor mediated pHi change, effects of Na+-H+ exchange, CI−-HCO3− exchange, Na+-HCO3− symport, and glycolysis blockers on the pHi change were examined. Results: Isoprenaline (1 μM) produced a decrease in pHi of 0.08(SEM 0.01) pH units and a transient depolarisation of the resting membrane. The isoprenaline induced intracellular acidosis was blocked by the β1 blocker atenolol (10 μM) but not by the β2 blocker ICI 118,551 (0.1 μM). Forskolin also produced a decrease in pHi of 0.06(0.03) pH units. In contrast, α adrenergic stimulation produced an increase in pHi, which was abolished by 1 mM amiloride, an Na+-H+ exchange blocker. In the presence of amiloride, the isoprenaline induced decrease in pHi was rather enhanced. 4,4'-Diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS, 1 mM), a blocker of CI−-HCO3−, exchange and the Na+-HC03− symport system, failed to affect the isoprenaline induced pHi decrease in bicarbonate buffered solution. However, pretreatment with 2-deoxyglucose or iodoacetic acid abolished the isoprenaline induced pHi decrease. Conclusions: β1 Adrenoceptor stimulation causes intracellular acidosis via the enhanced glycolysis, and the Na+-H+ exchange system appears to play a compensatory role. The β1 adrenoceptor mediated intracellular acidosis may modulate inotropic response to adrenergic stimulation in ventricular myocardium. Cardiovascular Research 1994; 28 :112-118 |
| Databáze: | OpenAIRE |
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