February 1, 1990Journal of Cardiovascular Pharmacology
Regional Vascular Resistance and Haemodynamics in the Spontaneously Hypertensive Rat
Population
Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY)
Comparison
Bradykinin administration vs Wistar-Kyoto rats (WKY)
Design
Preclinical
Authors
Discussion
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Implication
Does not inform clinical hypertension care; leaves open whether renal and skeletal muscle vasoconstriction drives human disease.
Key Points
- To identify which vascular beds contribute to elevated total peripheral resistance in spontaneously hypertensive rats compared with normotensive controls.
- Measured cardiac output distribution, organ blood flow, and regional vascular resistance using radiolabelled microspheres in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).
- Assessed regional haemodynamic responses to bradykinin to evaluate endothelium-derived relaxing factor-mediated vasodilation across organ beds.
- Total peripheral resistance was significantly elevated in SHR compared to WKY, despite both strains having similar heart rates, cardiac outputs, and stroke volumes.
- Vascular resistance was elevated across multiple organs in SHR, but reduced blood flow occurred selectively in renal and skeletal muscle beds.
- Bradykinin-induced responses were generally preserved between strains, except in the liver, where SHR exhibited no reduction in hepatic arterial resistance.
Structured PICO
P
Population
Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY)
I
Intervention
Bradykinin administration
C
Comparator
Wistar-Kyoto rats (WKY)
O
Outcome
Distribution of cardiac output, organ blood flow, and regional vascular resistance measured using radiolabelled microspheressurrogate
In spontaneously hypertensive rats, elevated total peripheral resistance is caused by widespread regional vascular resistance, particularly active vasoconstriction in renal and skeletal muscle beds.
Cite This Study
Thomas et al. (1990) studied this question.