Journal Name:
- Cerrahpaşa Tıp Dergisi
Key Words:
Keywords (Original Language):
| Author Name | University of Author | Faculty of Author |
|---|---|---|
Abstract (2. Language):
Although the regulatory role of
calcitonin released from the parafolicular cells of
thyroid gland and its essential role in the
haemoestasis of blood Ca2+ was well documented,
its effects on the physiological functions
of tissues except bones is not yet fully established.
Therefore, the aim of this study was to
explore, how calcitonin acts on the contractile
activity of heart and striated muscle.
Design and Results.- Experiments were carried
out on the isolated electrically driven left atria of
guinea-pigs and mice and phrenic nervediaphragm
preparations of rats. In the electrically
driven guinea-pig left atria (1 Hz, 2 msec, 2x
threshold voltage), contractility was depressed
by ampule calcitonin (Miacalcic) in a dosedependent
manner at concentrations in range of
0.25-4 μg/ml. This effect of ampule calcitonin
was weaker with respect to those produced by
the solvent being in the same amount. Especially
at 2 and 4μg/ml of ampule calcitonin, the contractile
response was biphasic, e.g. an initial
short-lived positive inotropic effect was preceding
the main negative inotropic one. Theophylline
(0.5 mM), atropine (2 μg/ml) and methylene
blue (2 μg/ml) antagonized ampule calcitonin
nonsignificantly, whereas the effect of solvent
remained unaltered. Verapamil (0.5 μg/ml), however,
augmented the negative inotropic effect of
both ampule calcitonin and the solvent. In the
phrenic nerve-diaphragm preparation, although
contractions induced by direct electrical stimulation
(0.1 Hz, 5 msec, 2x threshold voltage) was
depressed by ampule calcitonin dosedependently
in a concentration range of 1-8 μg/
ml, contractions induced by nerve stimulation
(0.1 Hz, 1 msec, 2x threshold voltage) was augmented
over a concentration of 4 μg/ml.
Conclusion.- Depending on these findings, it
was concluded that calcitonin has a stimulatory
effect on the contractile function of heart and striated
muscle which is masked by the solvent and
that cAMP, cGMP and Ca2+ channels all appeared
to involve in the cardiac effects of the
test agent.
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Abstract (Original Language):
Tiroid bezi parafoliküler hücrelerinden
salgılanan ve kan Ca2+ homeostazında ö-
nemli rol oynayan kalsitonin’in kalb ve
çizgili kas kasılması üzerine etkileri araştırılmıştır. Elektrikle uyarılan kobay solatriyumlannda (1 Hz, 2 msn, 2x eşik voltaj)
ampul kalsitonin (Miacalcic) 0.25-4
μg/ml konsantrasyon aralığında kasılmayı
doza-bağımlı bir şekilde deprese etmiştir.
Ampul kalsitonin’in bu etkisi, eşit hacimde
solventin oluşturduğu etkiden daha zayıftır. Özellikle, 2 ve 4 μg/ml konsantrasyonlarda
etki bifazikleşmektedir, yani asıl
negatif inotropik etkiye kısa ömürlü pozitif
intropik bir etki öncülük etmektedir.
Teofilin (0.5mM), atropin (2 μg/ml) ve
metilen mavisi (2 μg/ml) solventin etkisini
değiştirmediği halde, ampul kalsitonin’i
anlamsız da olsa antagonize etmiştir.
Verapamil (0.5 μg/ml) ise, hem
solvent ve hem de ampul kalsitonin’in negatif
inotropik etkisini artırmıştır. Frenik
sinir-diyafram pre paratõnda ampul
kalsitonin 1-8 μg/ml konsantrasyon aralığında direkt elektriksel uyarıya bağlı kasılmayı (0.1 Hz, 5 msn, 2x eşik voltaj) doza
bağımlı olarak deprese ederken, sinirsel
uyarıya bağlı kasılmada (0.1 Hz, 1
msn, 2x eşik voltaj) 4 μg/ml’den sonra artma
yapmıştır. Bu bulgulara dayanarak,
kalsitonin’in kasılmayı artırıcı bir etkisi
olduğu, bu etkinin solvent tarafından
maskelendiği ve kalpte kalsitonin’in etkisinde
cAMP, cGMP ve Ca2+ kanallarının
bir rolü olabileceği sonucuna varılmıştır.
FULL TEXT (PDF):
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