Blood Pressure in Genetically Hypertensive Rats

Publisher Website
Google Scholar
Abstract
Abstract We used a cross between the stroke-prone spontaneously hypertensive rat (SHRSP) strain and the Wistar-Kyoto (WKY) normotensive strain to elucidate the genetic basis of hypertension. Previous studies have reported conflicting evidence for the contribution of the Y chromosome to hypertension in these models. To investigate further the role of the Y chromosome in hypertension, we performed two large reciprocal crosses: one with the SHRSP as a male progenitor of the cross, yielding 60 F 2 rats, and another with the WKY as a male progenitor, yielding 83 F 2 rats. The resulting F 2 hybrids were phenotyped with the use of a radiotelemetry system (Data Sciences) for measurement of systolic, diastolic, and mean arterial pressures as well as heart rate and motor activity continuously for 96 hours at baseline and after 1% NaCl was added to the rats’ drinking water for 12 days. Male F 2 hybrids with the SHRSP grandfather had significantly higher average systolic, diastolic, and mean arterial pressures at baseline compared with male F 2 hybrids with the WKY grandfather (188.7±18.1 versus 168.9±11.5, 130.3±14 versus 115.7±7.3, and 159.1±15.8 versus 141.5±9.4 mm Hg, respectively). These differences were also observed after salt loading (197.9±22.1 versus 176.8±11.7, 136.5±17.3 versus 120.7±7.6, and 166.7±19.5 versus 148±9.7 mm Hg, respectively; P <.0001 for each comparison). These results suggest that the SHRSP Y chromosome contains a locus or loci that contribute to hypertension in SHRSP/WKY F 2 hybrids.