With the use of in vitro receptor autoradiography, this study aims at determining whether the higher level of kinin B2receptor density in the spinal cord of the spontaneously hypertensive rat (SHR) is secondary to arterial hypertension and whether chronic treatment with angiotensin I-converting enzyme inhibitors (ACEI) can regulate neuronal B1and B2receptors. SHR received, from the age of 4 wk, one of the two ACEI (lisinopril or zofenopril, 10 mg · kg−1· day−1) or for comparison, the selective AT1antagonist (losartan, 20 mg · kg−1· day−1) in their drinking water for a period of 4, 12, and 20 wk. Age-matched untreated SHR and Wistar-Kyoto rats (WKY) were used as controls. B2receptor binding sites in most laminae were higher in SHR than in WKY from the age of 8 to 24 wk. Whereas B1receptor binding sites were significantly present in young SHR and WKY, they were barely detectable in adult rats. ACEI (16 and 24 wk) and AT1antagonist (24 wk) enhanced the number of B2without changing B1receptor binding sites. However, at 8 wk the three treatments significantly increased B1and decreased B2receptors in lamina I. It is concluded that 1) the higher density of B2receptors 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) aging may have a profound impact on levels of B1and B2receptors in the rat spinal cord.