VOLUME-3, ISSUE-10
124
ADRENERGIC AND CALCIUM REGULATION OF CONTRACTILITY OF
NEONATAL RAT CARDIOMYOCYTES IN CULTURE
Maksimche a Galina Vladimi o na, Tsi e o a Na giza Aleksand o na,
Sabi o Ra shan Zai o ich
Ins i u e o Biophysics and Biochemis y
The s udy demons a ed ha ac i a ion o he ad ene gic sys em leads o an inc ease in he
equency o con ac ions due o s imula ion o bisop olol-sensi i e β₁-ad eno ecep o s. In
addi ion, neona al ca diomyocy es demons a ed di e en ial esponse o he calcium channel
an agonis ’s e apamil and ni edipine.
KEY WORDS: neona al ca diomyocy es, L- ype calcium channels, e apamil, ni edipine, β₁-
ad eno ecep o s, isop o e enol, bisop olol.
The p ima y ca diomyocy e cul u e acqui ed he abili y o con ac spon aneously on he
hi d day o cul i a ion. On he ou h day, he numbe o spon aneously con ac ing cells
accoun ed o mo e han 50% o he o al numbe o cells. The e o e, ou expe imen s we e
conduc ed on he 4 h day a e isola ion, and da a analysis was pe o med only on con ac ing
cells. Ca diomyocy es we e placed in a balanced Ty ode's saline solu ion, whe e he cells e ained
hei abili y o con ac spon aneously. The adminis a ion o isop o e enol, a syn he ic non-
selec i e β-ad ene gic agonis , led o a signi ican inc ease in he con ac ion equency o cells
o 179±17% (n=5) compa ed o he con ol. Howe e , when isop o e enol and bisop olol we e
used oge he , we obse ed a cell con ac ion equency o 127±11% (n=5), which was close o
he con ol alues and indica ed a blockade o he isop o e enol-media ed e ec due o inhibi ion
o β₁-ad eno ecep o s.
The ansmemb ane en y o Ca2+ ions in o ca diomyocy es is la gely ca ied ou h ough slow L-
ype calcium channels, which a e ac i a ed du ing memb ane depola iza ion and o m an ac ion
po en ial pla eau. Calcium an agonis s belong o class IV an ia hy hmics and a e capable o
supp essing ansmemb ane Ca²⁺ ion cu en . In ou expe imen s, e apamil a a concen a ion o
1 μM supp essed he equency o spon aneous con ac ions o ca diomyocy es by 92.0±2.3%
(n=10), while he same concen a ion o ni edipine supp essed i by only 47.6±16% (n=6). The
mo e p onounced e ec o e apamil may be associa ed no only wi h he blockade o L- ype
channels, bu also wi h i s abili y o in e ac wi h yanodine ecep o s (RyR2), educing he elease
o Ca²⁺ om he sa coplasmic e iculum [1]. Ou esul s a e consis en wi h he no ion ha
e apamil educes a io en icula conduc ion and supp esses sinus node au oma ici y [2],
whe eas ni edipine and o he dihyd opy idines ha e i ually no e ec on impulse conduc ion
h ough he AV node.
REFERENCES
1. Deng YL, Zhao JY, Yao JH, Tang Q, Zhang L, Zhou HL, Zhang CT, L JG, Quan XQ.
Ve apamil supp esses ca diac al e nans and en icula a hy hmias in acu e myoca dial ischemia
ia yanodine ecep o inhibi ion. Am J T ansl Res. 2017 Jun 15;9(6):2712-2722. PMID:
28670363; PMCID: PMC5489875.
2. Lang J., Timou Q., Lancon J.P., Aupe i J.F., Faucon G. (1988) Biphasic dose- esponse
ela ionship obse ed wi h Bay k 8644 on a io en icula nodal conduc ion inhibi ed by
e apamil. Naunyn Schmiedebe gs A ch Pha macol 338(2): 196-201. DOI: 10.1007/BF00174870
