Rettig R, Folberth C G, Graf C, Kopf D, Stauss H, Unger T
Pharmakologisches Institut, Universität Heidelberg.
Klin Wochenschr. 1991 Sep 3;69(13):597-602. doi: 10.1007/BF01649322.
Previous renal transplantation experiments in genetically hypertensive and normotensive rat strains indicated that a genetic defect in the kidney may be primarily involved in the pathogenesis of primary hypertension. In order to investigate whether this is also true for the most widely used animal model of primary hypertension, the spontaneously hypertensive rat (SHR), we performed renal transplantations using SHR and normotensive Wistar-Kyoto rats (WKY) as kidney donors and bilaterally nephrectomized F1 hybrids, bred from SHR x WKY parents as renal graft recipients. Our studies were also designed to differentiate between primary and secondary renal mechanisms as a possible cause of posttransplantation hypertension. Recipients of renal grafts from adult, naive SHR but not from adult normotensive WKY kidney donors developed posttransplantation hypertension. Permanent blood pressure normalization by antihypertensive treatment in adult SHR kidney donors and prehypertensive, young age of SHR kidney donors reduced, but did not prevent, posttransplantation hypertension. Increasing renal perfusion pressure in WKY kidney donors (2-kidney 1-clip hypertension) also resulted in posttransplantation hypertension in recipients of the non-clipped kidneys. Blood pressure remained normal in recipients of renal grafts from young WKY kidney donors. These data suggest that SHR kidneys carry a genetic defect which may be primarily involved in the pathogenesis of primary hypertension.
