Chronic hypertension impairs dilatation of cerebral arterioles. Impairment of dilatation generally has been attributed to hypertrophy of the vessel wall with encroachment on the vascular lumen. In this study, we tested the hypothesis that a reduction in external diameter may contribute to encroachment on the vascular lumen during chronic hypertension. We examined 10-12-month-old, anesthetized Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP). External diameter, stress, and strain of pial arterioles were calculated from measurements of pial arteriolar pressure (servo null), diameter, and cross-sectional area of the arteriolar wall. During maximal dilatation produced with ethylenediaminetetraacetic acid, cross-sectional area of the arteriolar wall was greater in SHRSP than in WKY rats (2,038 +/- 57 vs. 1,456 +/- 61 micron 2, p less than 0.05). External, as well as internal, diameter was less in SHRSP than in WKY rats (101 +/- 3 and 88 +/- 3 micron in SHRSP vs. 111 +/- 3 and 102 +/- 3 micron in WKY rats for external and internal diameter, respectively, p less than 0.05). Reduction in external diameter accounted for 76% of encroachment on the lumen in SHRSP, and hypertrophy per se accounted for only 24%. Distensibility of deactivated pial arterioles was increased in SHRSP. These findings suggest that reduction in external diameter plays an important role in impairment of maximal dilatation of cerebral arterioles in SHRSP, and reduction in vascular diameter in SHRSP cannot be accounted for by altered distensibility. We propose that, during chronic hypertension, cerebral arterioles undergo structural remodeling that results in a smaller external diameter and encroachment on the vascular lumen.(ABSTRACT TRUNCATED AT 250 WORDS)