Effects of praeruptorine C on the intracellular free calcium in normal and hypertrophied rat ventricular myocytes
Abstract
AIM: To study the intracellular free calcium ([Ca2+]i) in normal and hypertrophic
left ventricular myocytes isolated from adult rat hearts and the effects of
praeruptorine C (Pra-C) on them.
METHODS: [Ca2+]i of single myocyte was measured with Fura 2-AM.
RESULTS: The resting [Ca2+]i was 87 +/- 4 nmol.L-1 in normal left ventricular
myocytes, 123 +/- 7 nmol.L-1 in hypertrophied myocytes. After exposure to KCl
(20, 40, and 60 mmol.L-1), the [Ca2+]i were increased by 66%, 141%, and 268% in
normal myocytes, and 77%, 185%, and 243% in hypertrophic myocytes, respectively.
Pra-C (1, 10, and 100 mumol.L-1) concentration-dependently inhibited the [Ca2+]i
elevation caused by KCl (35 mmol.L-1) or norepinephrine (20 mumol.L-1) in both
normal and hypertrophied myocytes. All of the effects of Pra-C were similar to
that of nifedipine.
CONCLUSION: [Ca2+]i of hypertrophied myocytes was higher than that of normal ones
and Pra-C decrease the [Ca2+]i elevation in left ventricular myocytes resulted
from its calcium channel blockade.
Keywords:
left ventricular myocytes isolated from adult rat hearts and the effects of
praeruptorine C (Pra-C) on them.
METHODS: [Ca2+]i of single myocyte was measured with Fura 2-AM.
RESULTS: The resting [Ca2+]i was 87 +/- 4 nmol.L-1 in normal left ventricular
myocytes, 123 +/- 7 nmol.L-1 in hypertrophied myocytes. After exposure to KCl
(20, 40, and 60 mmol.L-1), the [Ca2+]i were increased by 66%, 141%, and 268% in
normal myocytes, and 77%, 185%, and 243% in hypertrophic myocytes, respectively.
Pra-C (1, 10, and 100 mumol.L-1) concentration-dependently inhibited the [Ca2+]i
elevation caused by KCl (35 mmol.L-1) or norepinephrine (20 mumol.L-1) in both
normal and hypertrophied myocytes. All of the effects of Pra-C were similar to
that of nifedipine.
CONCLUSION: [Ca2+]i of hypertrophied myocytes was higher than that of normal ones
and Pra-C decrease the [Ca2+]i elevation in left ventricular myocytes resulted
from its calcium channel blockade.