Key Points
- To determine whether flow-dependent dilatation is impaired in distal mesenteric arteries of spontaneously hypertensive rats compared with normotensive controls and evaluate the involvement of nitric oxide.
- Cannulated and pressurized distal mesenteric arterial segments from adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls to 80 mmHg to establish spontaneous myogenic tone.
- Assessed arterial diameter responses to incremental flow before and after incubation with the nitric oxide synthase inhibitor L-NAME, and before and after antibody-complement endothelial disruption.
- At a flow rate of 5 µL/min, arteries from WKY rats dilated significantly by 22 ± 5% (P < 0.01, n = 29), whereas arteries from SHR showed blunted dilatation of 4 ± 4% (not significant, n = 16).
- Incubation with L-NAME did not inhibit flow-induced dilatation in either strain, while endothelial disruption with antibody-complement abolished both flow- and acetylcholine-induced responses.
Structured PICO
PPopulationDistal mesenteric arteries from adult spontaneously hypertensive rats (SHR) (n=16) and normotensive Wistar-Kyoto rat (WKY) controls (n=29)
IInterventionIncremental flow increase, with and without NO synthase inhibitor L-NAME (and antibody-complement treatment in controls)
CComparatorNormotensive Wistar-Kyoto rat (WKY) controls
OOutcomeFlow-dependent dilatation (change in diameter)surrogate
Flow-dependent dilatation is impaired in distal mesenteric arteries from spontaneously hypertensive rats, which is endothelium-dependent but NO-independent, potentially contributing to increased peripheral resistance in hypertension.