Hypertension in cafeteria-fed rats: alterations in renal α2-adrenoceptor subtypes

• Published in: American journal of hypertension 2000-05, Vol.13 (5), p.529-534
• Main Authors: Coatmellec-Taglioni, Gwenn, Dausse, Jean-Pierre, Ribière, Catherine, Giudicelli, Yves
• Format: Article
• Language: English
• Subjects: Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood pressure; cafeteria diet; Cardiology. Vascular system; Experimental diseases; hypertension; Medical sciences; obesity; α2-adrenoceptor subtypes
• ISSN: 0895-7061; 1941-7225; 1879-1905
• DOI: 10.1016/S0895-7061(99)00234-4

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 α2-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 α2-adrenoceptor density that was solely due to an increased α2B-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 α2B-adrenoceptor subtype in these rats. On the other hand, despite a similar mRNA level, the α2A-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 α2-adrenoceptor distribution. These alterations, which are not related to genetic factors, may play a key role in the onset of hypertension.