High sodium intake has been associated with a higher blood pressure level. Resistance arteries are the main determinants of blood pressure. They are largely regulated by pressure (tensile stress)-induced tone (myogenic tone, MT) and by flow (shear stress)-induced dilation (FD). Thus, we studied the effect of NaCl (8%) intake for 8 weeks on FD and MT in mesenteric resistance arteries of spontaneously hypertensive rats. Arteries were cannulated and mounted in an arteriograph. Intraluminal diameter was measured continuously. High NaCl intake increased mean arterial pressure (186+/-5 to 217+/-6 mm Hg, P<0.01). Passive arterial diameter ranged from 112+/-6 to 185+/-9 microm (pressure from 25 to 125 mmHg, no effect of NaCl). MT developed in response to pressure (tone from 89+/-1% to 83+/-3% of passive diameter, 25 to 125 mm Hg). High NaCl intake significantly decreased MT (89+/-1% versus 83+/-3% of passive diameter when pressure was 125 mm Hg, P<0.023). High NaCl intake also decreased FD (6.5+/-0.8 versus 10+/-1.3 microm dilation under a pressure of 100 mm Hg and a flow rate of 160 microL/min, P<0.012). Thus, high salt intake decreased both flow (shear stress)-induced dilation and pressure (tensile stress)-induced tone in mesenteric resistance arteries. These findings might reflect attenuation by NaCl of flow and pressure mechanosensor processes.