We measured intracellular Ca2+ and isometric force simultaneously in endothelium-denuded mesenteric resistance arteries of 12- to 15-week-old male spontaneously hypertensive rats (SHR). Wistar-Kyoto (WKY) rats, and Wistar rats. Basal Ca2+ did not differ among vessels of these strains (SHR, 86.6 +/- 4.5 nmol/L; WKY, 78.5 +/- 4.7 nmol/L; Wistar, 83.1 +/- 3.9 nmol/L). Myofilament Ca2+ sensitivity was determined by measuring the intracellular Ca2+ and force responses to cumulative addition of extracellular Ca2+ (0.025 to 2.5 mmol/L) in the presence of 100 mmol/L K+ or 10 mumol/L norepinephrine after depletion of releasable intracellular Ca2+ stores. With 100 mmol/L K+, no between-strain differences in active stress, intracellular Ca2+, or myofilament Ca2+ sensitivity were observed. With 10 mumol/L norepinephrine, the active stress response of SHR vessels to 0.025 and 0.05 mmol/L Ca2+ was increased compared with both normotensive strains. The intracellular Ca2+ response was not different in vessels of SHR and WKY rats but was depressed in Wistar vessels. Myofilament Ca2+ sensitivity of SHR was elevated compared with both WKY and Wistar rats (P < .05) (ED25 for SHR, 74.4 +/- 5.1 nmol/L; WKY, 89.8 +/- 5.5 nmol/L; Wistar, 86.9 +/- 3.4 nmol/L). No strain differences in intracellular Ca2+ or active stress responses of SHR and WKY vessels were detected during cumulative addition of norepinephrine with constant extracellular Ca2+ (1.5 mmol/L). These results indicate that no hypertension-associated defect in vascular Ca2+ handling exists in mesenteric arteries of the SHR.(ABSTRACT TRUNCATED AT 250 WORDS)