Altered alpha 1-adrenoceptor subtypes mediated cardiac function after treatment of propranolol to rats
Abstract
AIM: To study inotropic and chronotropic effects mediated by alpha 1A- and alpha
1B-adrenoceptors after 5-d propranolol (Pro) treatment.
METHODS: The positive inotropic and chronotropic effects mediated by alpha 1A and
alpha 1B subtypes were determined on isolated left ventricular papillary muscles
and right atrium in Pro- and NaCl-treated rats.
RESULTS: The basic contractility of papillary muscles induced by phenylephrine
(Phe) was 90 +/- 18 mg in Pro-treated rats and 53 +/- 17 mg in control group (P <
0.05). The increment on force of contraction was 20 +/- 12 mg in Pro-pretreated
rats and 5 +/- 5 mg in NaCl-treated rats (P < 0.05). After preincubated with
chloroethylclonidine, the increment on force of contraction was reduced in
Pro-treated rats, but was not much changed in control group. Phe in presence of
5-methylurapidil induced positive inotropic effect with 13 +/- 5 mg in
Pro-treated group, but not in NaCl-treated rats. Under the normal and the
inhibited cardiac state, the maximal increment in beat rate mediated by alpha 1B
showed no difference between the Pro-treated and NaCl-treated rats.
CONCLUSION: After chronic treatment of Pro, alpha 1-adrenoceptor-mediated
positive inotropic effect in rat heart was improved, which was mainly induced by
stimulation of alpha 1B when beta-adrenoceptors were blocked.
Keywords:
1B-adrenoceptors after 5-d propranolol (Pro) treatment.
METHODS: The positive inotropic and chronotropic effects mediated by alpha 1A and
alpha 1B subtypes were determined on isolated left ventricular papillary muscles
and right atrium in Pro- and NaCl-treated rats.
RESULTS: The basic contractility of papillary muscles induced by phenylephrine
(Phe) was 90 +/- 18 mg in Pro-treated rats and 53 +/- 17 mg in control group (P <
0.05). The increment on force of contraction was 20 +/- 12 mg in Pro-pretreated
rats and 5 +/- 5 mg in NaCl-treated rats (P < 0.05). After preincubated with
chloroethylclonidine, the increment on force of contraction was reduced in
Pro-treated rats, but was not much changed in control group. Phe in presence of
5-methylurapidil induced positive inotropic effect with 13 +/- 5 mg in
Pro-treated group, but not in NaCl-treated rats. Under the normal and the
inhibited cardiac state, the maximal increment in beat rate mediated by alpha 1B
showed no difference between the Pro-treated and NaCl-treated rats.
CONCLUSION: After chronic treatment of Pro, alpha 1-adrenoceptor-mediated
positive inotropic effect in rat heart was improved, which was mainly induced by
stimulation of alpha 1B when beta-adrenoceptors were blocked.