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Carotid artery hemodynamics and vasomotor function in hypertensive and normotensive rats

To investigate the effect of hypertension on common carotid artery (CCA) hemodynamics and vasomotor function, we measured blood flow and pressure in the left‐CCA of 20wk old male anesthetized spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) and Sprague Dawley (SD) rats, followed by in vitro vasomotor function testing on excised phenylephrine‐preconstricted right‐CCA rings in response to cumulative acetylcholine (ACh) and sodium nitroprusside (SNP). CCA blood flow was 30–40% lower and more oscillatory in SHR compared to WKY and SD (p<0.01), whereas SHR blood pressure was much higher resulting in a markedly decreased vascular conductance (p<0.01). CCA endothelial‐mediated dilation to ACh was blunted in SHR compared to WKY and SD (p<0.01); moreover, higher doses of ACh produced a 27±4% ‘re‐constriction’ in rings from SHR that persisted when blocking nitric oxide synthase (p<0.01). Interestingly, non‐specific blockade of cyclooxygenase reversed this ACH‐induced constriction in SHR and improved dilation to the level of WKY and SD (p<0.01). Endothelium‐independent dilation to SNP was similar between SHR and WKY, and augmented at sub‐max doses in SD (p<0.01). These data suggest that hypertension is associated with low/oscillatory blood flow and prostaglandin‐mediated endothelial vasomotor dysfunction in the CCA.