Enhanced arteriolar vasomotion in rats with chronic salt-induced hypertension.

The aims of this study were (1) to determine if the establishment of hypertension in the Dahl salt-sensitive (DS) rat is accompanied by alterations in arteriolar vasomotion and (2) to explore the influence of endogenous nitric oxide on vasomotion in normotensive and hypertensive DS rats. Rhythmic diameter changes of arcading arterioles were studied in the superfused spinotrapezius muscle of DS fed high (4%) or low (0.45%) salt diets for 6 weeks. Mean arterial pressure for DS on high salt (166 +/- 7 mm Hg) was significantly greater than that for DS on low salt (131 +/- 9 mm Hg). There was no difference between hypertensive and normotensive DS in time-averaged arteriolar diameter, vasomotion frequency, or vasomotion cycle length. However, average vasomotion amplitude was 93% greater in hypertensive DS than in normotensive DS. Inhibition of nitric oxide synthesis with NG-Nitro-L-arginine methyl ester did not alter vasomotion in hypertensive DS, but increased vasomotion amplitude in normotensive DS to a level not different from that in hypertensive DS. L-Arginine had no effect on vasomotion in either group. Therefore, cyclic variations in arcade arteriole diameter are normally limited by basal nitric oxide, and the enhancement of these variations in animals with salt-induced hypertension may be attributable to the loss of this nitric oxide influence. The increased vasomotion amplitude and unchanged average diameter in hypertensive DS suggests a reduced hydraulic resistance within this particular segment of the arteriolar network.