PMID- 10087147
OWN - NLM
STAT- MEDLINE
DCOM- 19990604
LR  - 20190726
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 437
IP  - 5
DP  - 1999 Apr
TI  - Adrenoceptor-mediated regulation of myofibrillar Ca2+ sensitivity through the 
      GTP-binding protein-related mechanisms: tension recording in beta-escin-skinned 
      single rat cardiac cells with preserved receptor functions.
PG  - 702-9
AB  - To investigate the mechanisms of receptor-mediated regulation of heart muscle 
      contraction, we developed a tension-recording system using beta-escin-skinned 
      single cardiac cells of rats and studied the effects of agonists on myofibrillar 
      Ca2+ sensitivity and Ca2+ release from the sarcoplasmic reticulum (SR). In 
      pCa/tension relations, 1 microM isoproterenol plus 100 microM guanosine 
      5'-triphosphate (GTP) decreased the myofibrillar Ca2+ sensitivity (pCa50, the 
      [Ca2+] required for half-maximal tension, as an indicator of the sensitivity; 
      from 6.07 to 5.92); this effect was blocked by 1 microM metoprolol or 1 mM 
      guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS). Phenylephrine (10 microM) plus 100 
      microM GTP increased the Ca2+ sensitivity (pCa50; from 6.12 to 6. 28), and this 
      effect was blocked by 1 microM phentolamine or 1 mM GDPbetaS. After Ca2+ loading 
      into the SR, 10 microM phenylephrine plus 100 microM GTP in a low-ethylene- 
      glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA, 0. 1 mM) 
      relaxing solution induced oscillatory contractions that were attenuated by either 
      1 microM phentolamine or pre-treatment with 10 microM inositol 
      1,4,5-trisphosphate. Our results demonstrate that beta1-adrenergic stimulation 
      decreases myofibrillar Ca2+ sensitivity and that alpha1-adrenergic stimulation 
      both increases the Ca2+ sensitivity and activates Ca2+ release from the 
      agonist-sensitive SR through GTP-binding protein-related mechanisms.
FAU - Satoh, S
AU  - Satoh S
AD  - Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu 
      University School of Medicine, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, 
      Japan.satoshin@cardiol.med.kyushu-u.ac.jp
FAU - Kinugawa, S
AU  - Kinugawa S
FAU - Tsutsui, H
AU  - Tsutsui H
FAU - Takeshita, A
AU  - Takeshita A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Adrenergic Agonists)
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Receptors, Adrenergic)
RN  - 1WS297W6MV (Phenylephrine)
RN  - 6805-41-0 (Escin)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adrenergic Agonists/pharmacology
MH  - Adrenergic alpha-Agonists/pharmacology
MH  - Animals
MH  - Calcium/*pharmacology
MH  - Calcium Signaling/drug effects
MH  - Escin/pharmacology
MH  - GTP-Binding Proteins/*physiology
MH  - Heart/drug effects
MH  - Heart Ventricles/cytology/drug effects
MH  - In Vitro Techniques
MH  - Male
MH  - Muscle Contraction/physiology
MH  - Myocardial Contraction/drug effects/*physiology
MH  - Myocardium/*cytology/metabolism
MH  - Myofibrils/drug effects/*physiology
MH  - Phenylephrine/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Adrenergic/drug effects/*physiology
MH  - Sarcoplasmic Reticulum/drug effects
MH  - Ventricular Function
EDAT- 1999/03/23 00:00
MHDA- 1999/03/23 00:01
CRDT- 1999/03/23 00:00
PHST- 1999/03/23 00:00 [pubmed]
PHST- 1999/03/23 00:01 [medline]
PHST- 1999/03/23 00:00 [entrez]
AID - 10.1007/s004240050835 [doi]
PST - ppublish
SO  - Pflugers Arch. 1999 Apr;437(5):702-9. doi: 10.1007/s004240050835.