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Titlebook: Essential Hypertension 2; Kyuzo Aoki Book 1989 Springer Japan 1989 hypertension

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Decreased α1-Adrenoceptor Reserve in Arteries from Spontaneously Hypertensive Ratsensive rats (Aoki SHR, 13 weeks old, male) and age- and sex-matched normotensive Wistar-Kyoto rats (WKY). The α-adrenoceptor agonist, phenylephrine, caused dose-dependent contractions of the strips from both strains. The SHR strips developed a greater tension with a smaller pD. value as compared wit
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Excitatory Agonists and Ca-Permeable Channels in Arterial Smooth Muscle Cellsaction, are consistent with a limited role of Ca entry during norepinephrine stimulation. ATP (10. – 10. .) activates a transient inward current at a holding potential of −60 mV in chemically dispersed, single smooth muscle cells. The reversal potential of this current and its modification by ionic
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Relationship Between Cytosolic Calcium Level and Contractile Tension in Vascular Smooth Muscleanges due to high K.. Although verapamil inhibited the [Ca.]. stimulated by receptor-agonists and phorbol esters to the resting level, a portion of the sustained contraction was not inhibited. In Ca.-free solution, norepinephrine, prostaglandin F., caffeine, or ionomycin induced only a transient inc
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Calcium Mobilization Mechanisms in Smooth Muscleboth CICR and IICR, but the remainder (Sβ) was only with IICR and not with CICR. This heterogeneity was confirmed by using ryanodine, which specifically acts on the CICR mechanism to fix the CICR channel in an open state. Thus, after ryanodine treatment, Sa no longer accumulated calcium but Sβ did.
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Sarcoplasmic Reticulum of Mesenteric Arteries Buffers Stimulated Ca2+ Entrymplitude of half the magnitude of the rapid monophasic contraction induced by caffeine. It is concluded that norephinephrine potentiates the contractile effect of Ca. entry in mesenteric arteries by shunting out the superficial buffer barrier.
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