Qiu H Y, Henrion D, Levy B I
Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Paris VII, Hôpital Lariboisière, France.
Hypertension. 1994 Oct;24(4):474-9. doi: 10.1161/01.hyp.24.4.474.
We studied the effect of endothelium on the flow-induced response of conductance arteries and the resistance arteriolar network in an in situ model of perfused mesenteric artery in normotensive Wistar-Kyoto and spontaneously hypertensive rats. The mesenteric network was perfused with a Tyrode's albumin solution. The diameter of a conductance mesenteric artery was measured using a video camera system, and mesenteric pressure was recorded in a collateral artery. The preparation was perfused at 0.2, 2, and 4 mL/min, and flow-diameter-pressure relations were established (1) under control conditions, (2) during local inhibition of nitric oxide synthesis by topical application of N omega-nitro-L-arginine methyl ester (L-NAME) (1 mmol/L), and (3) after endothelium removal (CO2 drying). In normotensive rats, L-NAME decreased conductance artery diameter by 12 +/- 2% (P < .01) at 0.2 mL/min and 3.3 +/- 1.9% (P < .05) at 2 mL/min. In hypertensive rats, L-NAME did not modify mesenteric diameter. Endothelium removal markedly increased arterial resistance in both strains and decreased conductance artery diameter in normotensive rats (10.3 +/- 3%, P < .05 at 0.2 mL/min and 4.2 +/- 2%, P < .05 at 2 mL/min) but not in hypertensive rats. The present study suggests that the endothelium plays a similar role in the control of mesenteric resistance in both strains and that there is a significant diameter-flow dependency affected by both endothelium removal and inhibition of nitric oxide synthesis in conductance mesenteric arteries from normotensive but not from hypertensive rats.
