Cellular calcium movements and the role in regulating contraction and relaxation of vascular smooth muscles of resistance vessels

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We investigated the cellular Ca^<2+> Movement and its role in regulation of contractions and relaxations in vascular smooth muscles of resistance vessels. Major aidings are as follows.1. Relation of transmembrane Ca^<2+> influx to intracellular Ca^<2+> release. Based on the sensitivity to ryanodine of Ca^<2+>-induced contraction of rat mesenteric resistance vessels which had been depolarized by 40mMK^+, Ca^<2+>-free medium, it has been shown that Ca^<2+> influx through Ca^<2+> Channels triggers that Ca^<2+> release from sarcoplasmic reticulum. This mechanism may be physiologically important since it amplifies the threshold level of contraction to half maximal one. On the other hand, in resting state, the sarcoplasmic reticulum plays a role as a sink to buffer cytoplasmic Ca^<2+>. Removal of this function by ryanodine induced a tension development. 2. Increased level of cytoplasmic Ca^<2+> at resting state in hypertensive vessels and activation of Ca^<2+>-dependent K^+ channel. Femoral … More and carotid arterie s from spontaneously hypertensive rats(SHR)showed a greater decrease in tension in response to Ca^<2+>-removal from bathing solution or Ca^<2+> channel blockers and greater contractile responses to charybdotoxin and TEA, Ca^<2+>-activated K^+ channel blockers, than those from normotensive rats. Measurement of cytoplasmic Ca^<2+> with fura-2 revealed that the resting level of cytoplasmic Ca^<2+> was higher in SHR vessels. Resting membrane potential did not differ between hypertensive and normotensive vessels. It is suggested that Ca^<2+> easily enters cells in SHR vessels at resting state, thereby produces the active tension and activates Ca^<2+>-activated K^+ channels.3. The nature of tonic contraction induced by alpha-adrenoceptor activation. We analyzed the tonic contraction induced by phenylephrine, alpha1 receptor agonist, and found that the contraction was composed of two components, one is related to activation of protein kinase C and the other depends on Ca^<2+> influx through L-type Ca^<2+> channels. The former may cause an increase in the sensitivity to Ca^<2+> of contractile systems. It is under investigation whether the same mechanism underlies the alpha1-adrenoceptor mediated contraction of resistance vessels. Less