Cardiac plasma membrane physical properties and β-adrenergic receptor function are unaltered in portal-hypertensive rats
✍ Scribed by Zenghua Ma; Jonathan B. Meddings; Samuel S. Lee
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 720 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
We have previously demonstrated that impairment of cardiac contractility in a rat model of cirrhosis may be secondary to altered cardiac plasma membrane physical properties affecting p-adrenergic receptor function. It is unclear whether this is caused by the cirrhosis or by the portal hypertension in this model, so we studied cardiomyocyte plasma membrane physical properties, lipid composition, and p-adrenergic receptor function in a rat model of prehepatic portal hypertension without cirrhosis. Portal hypertension was induced by graded portal vein stenosis, whereas controls had a sham operation. Cardiac sarcolemmal plasma membrane physical properties were studied by fluorescent polarization methods using diphenylhexatriene and a series of an- throyloxy-stearic acids to estimate, respectively, the static and dynamic components of membrane fluidity. p-Adrenergic receptor density and binding affinity were measured using 3H-dihydroalprenolol as a radioligand. Isoproterenol-stimulated adenylyl cyclase activity was measured by radioimmunoassay. Neither the static nor the dynamic components of membrane fluidity were significantly different in portal-hypertensive rats compared with the controls. The membrane cholesterol, phospholipid content, and the cholesteroYphospholipid ratio did not differ between the two groups. p-Adrenergic receptor density and binding affinity in the portalhypertensive rats (respectively, 1.65 ? 0.06 pmoYmg protein and 6.78 ? 0.80 nmol/L) were not different from controls (1.76 ? 0.17 pmoYmg protein and 7.25 -C 1.48 nmol/L). Isoproterenol-stimulated adenylyl cyclase activity in membranes from portal-hypertensive rats did not significantly differ from controls. We conclude that cardiac plasma membrane physical properties and padrenoceptor function in portal hypertensive rats remains unimpaired, suggesting that the cardiomyopathy