Key Points
- To identify structural differences in the renin gene between stroke-prone spontaneously hypertensive rats and normotensive controls, and to assess whether these alterations correlate with cardiovascular phenotypes.
- Conducted restriction fragment length polymorphism analysis using hybridization against defined renin gene probes in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto (WKY) rats.
- Evaluated genotype-phenotype cosegregation in an F2 hybrid cross-bred cohort (n = 115) using direct conscious arterial blood pressure monitoring, stress testing, dietary sodium loading, and organ weight measurements.
- Identified an approximate 700-base-pair deletion within the first intron of the renin gene in SHRSP compared to WKY rats, localized to a multimeric tandem repeat region.
- Found no cosegregation of the renin genotype with systolic or diastolic blood pressure, heart rate, stress-induced or sodium-induced blood pressure changes, plasma renin activity, or ventricular hypertrophy in F2 hybrid rats.
Structured PICO
PPopulationStroke-prone spontaneously hypertensive rats (SHRSP), normotensive Wistar-Kyoto rats (WKY), and F2 hybrid rats (n=115)
IInterventionGenotype analysis (renin gene restriction fragment length polymorphism)
CComparatorNormotensive control (WKY) and different genotypes in F2 hybrids
OOutcomeCosegregation of systolic or diastolic blood pressure with renin genotypesurrogate
A structural difference in the renin gene between SHRSP and WKY rats does not cosegregate with blood pressure or other cardiovascular phenotypes in F2 hybrids, suggesting differential roles of the renin-angiotensin system in different models of genetic hypertension.