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Hypertension in cafeteria-fed rats: alterations in renal 2-adrenoceptor subtypes
Obesity is a major cause of human essential hypertension and there are clear evidences that abnormal kidney functions play a key role in obesity hypertension. Feeding rats a cafeteria diet has been extensively used as an experimental model to study obesity and energy balance expenditure. The present...
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Published in: | American journal of hypertension 2000-05, Vol.13 (5), p.529-534 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Obesity is a major cause of human essential hypertension and there are clear evidences that abnormal kidney functions play a key role in obesity hypertension. Feeding rats a cafeteria diet has been extensively used as an experimental model to study obesity and energy balance expenditure. The present study investigated whether rats fed a cafeteria diet develop hypertension with alterations in renal alpha2-adrenoceptor subtype distribution. Weight gain induced by feeding rats a cafeteria diet during 8 weeks was associated with a marked increase in blood pressure. Insulin levels were higher in these hypertensive rats, leading to a decreased plasma glucose/insulin ratio. Based on radioligand-binding studies using [3H]-RX821002 and selective competitors, a raise in alpha2-adrenoceptor density that was solely due to an increased alpha2B-adrenoceptor subtype density was detected in the kidney of the cafeteria-fed rat. Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) experiments showed an overexpression of the gene encoding the alpha2B-adrenoceptor subtype in these rats. On the other hand, despite a similar mRNA level, the alpha2A-adrenoceptor subtype was no more detectable by radioligand-binding studies in the kidney of the cafeteria-fed rat. In conclusion, cafeteria-fed rats are hypertensive, with renal alterations in alpha2-adrenoceptor distribution. These alterations, which are not related to genetic factors, may play a key role in the onset of hypertension. |
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ISSN: | 0895-7061 1941-7225 |
DOI: | 10.1016/S0895-7061(99)00234-4 |