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(Hypertension. 1995;25:110-116.)
© 1995 American Heart Association, Inc.

Articles

Myofilament Calcium Sensitivity of Normotensive and Hypertensive Resistance Arteries

Ka Bian; Richard D. Bukoski

From the Hypertension and Vascular Research Laboratories, Department of Internal Medicine, University of Texas Medical Branch, Galveston Island.

Correspondence to Richard Bukoski, PhD, Hypertension and Vascular Research Laboratories, J-65, University of Texas Medical Branch, Galveston Island, TX 77550.

Abstract 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 µmol/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 µmol/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. Moreover, although resistance arteries of SHR exhibit enhanced myofilament Ca²⁺ sensitivity compared with two normotensive strains after depletion of intracellular Ca²⁺ and activation with 10 µmol/L norepinephrine, this difference is not observed under the more physiological manipulation of cumulative addition of norepinephrine in the presence of constant Ca²⁺. We conclude that enhanced myofilament Ca²⁺ sensitivity is unlikely to contribute to the hypertension of SHR.

Key Words: hypertension, genetic • muscle, smooth, vascular • fura 2 • calcium • vascular resistance

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