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1 Department of Physiology, University of Montreal, Montreal, Quebec, Canada
2 Department of Pharmacology, University of Montreal, Montreal, Quebec, Canada
3 Department of Pharmacology, University of Sherbrooke, Sherbrooke, Quebec, Canada
4 Clinical Research Institute, University of Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: couturer{at}physio.umontreal.ca.
Using in vitro receptor autoradiography, this study aims at determining whether the higher level of kinin B2 receptor density in the spinal cord of SHR is secondary to arterial hypertension, and if chronic treatment with angiotensin-1 converting enzyme inhibitors (ACEI) can regulate neuronal B1 and B2 receptors. SHR received from the age of 4 weeks, one of the two ACEI (lisinopril or zofenopril, 10 mg/kg/day ) or for comparison, the selective AT1 antagonist (losartan, 20 mg/kg/day) in their drinking water for a period of 4, 12 and 20 weeks. Age-matched untreated SHR and Wistar Kyoto rats (WKY) were used as controls. B2 receptor binding sites in most laminae were higher in SHR than in WKY from the age of 8 to 24 weeks. While B1 receptor binding sites were significantly present in young SHR and WKY, they were barely detectable in adults. ACEI (16 and 24 weeks) and AT1 antagonist (24 weeks) enhanced the number of B2 without changing B1 receptor binding sites. However, at 8 weeks the three treatments significantly increased B1 and decreased B2 receptors in lamina I. It is concluded that I) the higher density of B2 receptors in the spinal cord of SHR is not due to hypertension, 2) kinin receptors are regulated differently by ACEI in neuronal and vascular tissues, and 3) ageing may have a profound impact on levels of B1 and B2receptors in the rat spinal cord.
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