ABSTRACT
Objective To compare the effects of ouabain and digoxin on both the systolic blood pressure (SBP) and sodium pump α-subunit expression in myocardium of rats. Methods Normal Sprague-Dawley (SD) rats were injected with ouabain, digoxin or normal saline (NS) everyday and indirect SBP was recorded once a week. Six weeks later, all the rats were killed and sodium pump α1-, α2-, and α3-subunit were detected in the left ventricular myocardium with RT-PCR method and immunohistochemical assay at mRNA and protein levels. Results At the end of six weeks SBP of rats infused with ouabain increased significantly (132.6±9.0 vs 115.7±8.2 mm Hg， P＜0.01), while no difference of SBP was found between digoxin group and NS group. The effects of ouabain and digoxin on sodium pump α-subunit isoform expression in myocardium were also different: both ouabain and digoxin stimulated expression of α3-isoform whereas α2-isoform unchanged at both mRNA and protein levels. α1-isoform was decreased in ouabain group and α1-isoform unchanged in digoxin group at both mRNA and protein levels. Conclusion It is suggested that both ouabain and digoxin could regulate sodium pump α-subunit isoform expression, which might be related to the physiological roles of endogenous ouabain and might be responsible for the difference between the pharmacological and toxicological effects of ouabain and digoxin, including their effects on blood pressure.
ABSTRACT
Objective To investigate the gene expression of sodium pump α-subunit in aortic smooth muscle of 1-kidney-1-clip (1k1c) hypertensive rats. Methods 1k1c hypertensive rats were prepared by partially ligating the left renal artery and removing the right kidney. 4 weeks later, all the rats were killed and sodium pump α1- , α2-, and α3-subunit in aortic smooth muscles were detected with reverse transcription p ol ymerase chain reaction (RT-PCR) method and immunohistochemical assay at both mR NA and protein levels, respectively. Resulsts Changes in the expression of sodi um pump α-subunit gene were found in aortic smooth muscles of 1k1c hypertensiv e rats: α1-su bunit increased at both mRNA protein levels, while α2- and α3-subunits r emained without changes. Conclusions There were great changes in the gene expression of so dium pump α-subunit in aor tic smooth muscles of 1k1c hypertensive rats, which might be related to the development of hypertension in this hypertensive model.
ABSTRACT
Objective To compare the effects of ouabain and digoxin on both the systolic blood pressure and sodium pump α-subunit isoforms gene expression in the aortic smooth muscle of rats. Methods Normal SpragueDawley rats were injected with ouabain (20μg·kg-1 ·d-1 ,i. p),digoxin (32 μg·kg-1 ·d-1,i. p)and normal saline once a day, respectively, and indirect systolic blood pressure was recorded once a week. Six weeks later,all the rats were killed and sodium pump α1-,α2-,and α3-subunit mRNA levels were detected in the aortic smooth muscle with reverse transcription polymerase chain reaction(RT-PCR) method. Results The systolic blood pressure of rats infused with ouabain increased significantly at the end of week 6 [132. 6± 9. 0 mmHg (1 mmHg ＝ 0. 133 kPa)vs 115. 7±8.2mmHg, P ＜0. 01] ,while no difference of blood pressure was found between digoxin group and NS group (P＞0.05).The expression of sodium pump α-subunit isoforms in aortic smooth muscle was regulated by either ouabain or digoxin:both ouabain and digoxin increased α1- and α3-subunit expression, α2-subunit decreased in digoxin group but unchanged in ouabain group. Conclusion These results suggest that both ouabain and digoxin could regulate sodium pump α-subunit isoform expression, which might be related to the physiological roles of endogenous ouabain and might be responsible for the difference between the pharmacological and toxicological effects of ouabain and digoxin,including their effects on blood pressure.
ABSTRACT
ObjectiveTo explore the distribution of sodium pump α-subunit isoforms at both mRNA and protein level in normal Sprague-Dawley(SD) rats. MethodsWith RT-PCR (reverse transcription-polymerase chain reaction) and immunohistochemical assay, sodium pump α1-, α2-, andα3-subunit isoforms were detected at mRNA level and protein level in the myocardium, liver, kidney, adrenal gland, aortic smooth muscle, pituitary and hypothalarnus in normal rats. ResultsSodium pump α1-, α2-, and α3-subunit isoforms distribute in a tissue-specific fashion in normal SD rats. α1 and α2 are the main isoforms and α3 is much less in myocardium. α1 is more than α2 or α3 isoform at mRNA level in liver, while all of α1-,α2-, and α3-isoform are less expressed at protein level. α1-isoform is abundantly but α2 and α3 are less expressed both at mRNA and protein levels in kidney. α2isoform is just more than α1 and α3 isoforms in aortic smooth muscle. All of three isoforms are expressed abundantly in pituitary. α2 and α3 are more and α1 is less expressed in hypothalamus. ConclusionThe results of this study have revealed the distribution of sodium pump α-subunit isoforms at both mRNA and protein level in normal SD rats, which might be helpful for the further studying the physiologic and pathologic roles of sodium pump.
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Objective To explore the relationship between endogenous ouabain and the pathogenesis of hyper- tension. Methods ① Sixteen Sprague-Dawley (SD) rats were selected and randomly divided into two groups, and then the rats were injected with ouabain in dosage of 20μg/kg. d and normal saline (NS), respectively. The indirect systolic blood pressure of all the rats were recorded once a week. ②) Twenty-five lk1c (one kidney and one clipped) hypertensive rats were established and injected randomly with anti-ouabain antibody, normal rabbit IgG and normal saline, respectively. The direct blood pressure of all the lklc hypertensive rats were recorded by cannulated carotid artery for 3h after administration. Results The systolic blood pressure of rats injected with ouabain began to increase 2 weeks after ouabain administration and increased significantly at 6 weeks compared with NS group (17.7±1.2)kPa vs .(15.4±1.1)kPa, P＜ 0. 01). Anti-ouabain antibody could significantly decrease the blood pressure of 1 k1c rats, while the normal rabbit IgG could not. ConclusionThe results of this study indicate that endogenous ouabain might be one of the pathogenetic factors of hypertension.
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AIM: To explore the role of endogenous ouabain (EO) in the development of hypertension and its secretion character in 1k1c hypertensive rats(HR). METHODS: EO contents of plasma and tissues in 1k1c HR were detected by ELISA. The relationships between plasma and tissues ouabain and blood pressure were analyzed. RESULTS: EO contents of plasma, heart, kidney, adrenal gland, pituitary and hypothalamus in lklc HR were significantly higher than those of normal rats, especially in the adrenal gland and hypothalamus. EO contents of serum, kidney and hypothalamus were correlated with blood pressure. CONCLUSIONS: EO might play an important role in the development of hypertension in 1k1c hypertensive rats. Adrenal gland might be the major source of EO.
ABSTRACT
AIM: To investigate the regulation of sodium pump ?-subunit gene expression in the cortex of kidneys from one kidney one clip (1k1c) hypertensive rats. METHODS: 1k1c hypertensive rats were prepared by partially ligating the left renal artery and removing the right kidney. 4 weeks later, all the rats were killed, the levels of sodium pump ? 1-, ? 2-, and ? 3-subunit mRNA and protein in the cortex of kidney were detected with reverse transcription polymerase chain reaction (RT-PCR) method and immunohistochemical assay, respectively. RESULTS: The mRNA levels of sodium pump ? 1-subunit increased and ? 2- and ? 3-subunit were unchanged in the cortex of kidneys from 1k1c hypertensive rats compared with control rats, while no change has been found for all the three subunits gene expressions at protein level. CONCLUSION: There were some changes in the expression of sodium pump ?-subunit gene in the cortex of kidney of the 1k1c hypertensive rat, which might be related to the development of hypertension in this hypertensive model.