Key Points
- To determine whether spontaneously hypertensive rats display altered pressor and renal vascular responses to angiotensin II and whether converting enzyme inhibition can reverse these abnormalities.
- Evaluated systemic pressor responses and renal blood flow using an electromagnetic flowmeter across graded angiotensin II doses (5–300 ng) in 24 spontaneously hypertensive rats (SHR) and 24 Wistar-Kyoto rats (WKY) fed a 1.6% sodium diet.
- Administered the converting enzyme inhibitor captopril (1–30 mg/kg) to compare systemic versus intrarenal converting enzyme blockade between rat strains.
- Baseline blood pressure was significantly elevated in SHR compared to WKY (155 ± 4 vs. 106 ± 2 mm Hg; p < 0.001), while baseline renal blood flow was lower (6.9 ± 0.5 vs. 8.2 ± 0.4 ml/min/g; p < 0.05).
- Angiotensin II induced an enhanced systemic pressor response (p < 0.0005) but a blunted renal vascular response (p < 0.005) in SHR relative to WKY controls.
- Captopril reduced blood pressure more in SHR than WKY, increased renal blood flow in both strains, and reversed the blunted renal vascular response in SHR, though maximum renal enzyme inhibition required higher doses than systemic inhibition.
Structured PICO
PPopulation24 spontaneously hypertensive rats (SHR) and 24 Wistar-Kyoto rats (WKY) ingesting 1.6% Na
IInterventionGraded angiotensin II doses (5-300 ng) and captopril (1-30 mg/kg)
CComparatorWistar-Kyoto rats (WKY) as normotensive controls
OOutcomeRenal blood flow and pressor responses to graded ANG II dosessurrogate
The blunted renal vascular response to angiotensin II in spontaneously hypertensive rats is reversed by captopril, suggesting inappropriate intrarenal ANG II formation.