1980
DOI: 10.1161/01.res.46.3.372
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Membrane electrical effects of histamine on vascular smooth muscle of canine coronary artery.

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Cited by 27 publications
(8 citation statements)
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References 15 publications
(16 reference statements)
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“…According to whole-tissue experiments with intracellular microelectrodes, mammalian coronary arteries are electrically unexcitable unless TEA is applied, in which case calcium spikes occur in the normally quiescent tissue. 21 These observations suggest that electrical excitability and possibly contractility of the coronary smooth muscle cell membrane is strongly regulated by a TEA-sensitive K + conductance.…”
Section: Outward Potassium Currents In Freshly Isolated Smooth Musclementioning
confidence: 88%
“…According to whole-tissue experiments with intracellular microelectrodes, mammalian coronary arteries are electrically unexcitable unless TEA is applied, in which case calcium spikes occur in the normally quiescent tissue. 21 These observations suggest that electrical excitability and possibly contractility of the coronary smooth muscle cell membrane is strongly regulated by a TEA-sensitive K + conductance.…”
Section: Outward Potassium Currents In Freshly Isolated Smooth Musclementioning
confidence: 88%
“…Histamine stimulation of arterial smooth muscle usually causes an initial rapid phase of contraction thought to correspond to the release of Ca ++ from internal stores, and a slower tonic phase thought to reflect the entry of Ca ++ from the extracellular space (Hudgins and Weiss, 1968;Watkins and Davidson, 1980 (Harder, 1980 ] o , was less than 1.2 ITIM. Potassium-free solutions usually depolarize vascular smooth muscle, whether through inhibition of an electrogenic Na-K pump, a decrease in potassium conductance, or indirectly, through norepinephrine release from nerve endings (for a review, see Hermsmeyer, 1983).…”
Section: Discussionmentioning
confidence: 99%
“…Apparently, high-K + per se does not inhibit aerobic glycolysis as long as [Na + ]0 is not reduced. While the addition of histamine to K + -substituted saline (reduced [Na + ] o ) stimulates aerobic glycolysis, this could nonetheless be an effect of [Na + ]0, since histamine has been suggested to increase membrane permeability to Na + , as well as Ca ++ and K + (Casteels and Suzuki, 1980;Harder, 1980). The Ca ++ -sensitive excess ATPase induced by histamine might then reflect increased Ca ++ extrusion via a Na + / Ca ++ exchange mechanism (cf Lang and Blaustein, 1980) powered by the Na + /K + ATPase.…”
Section: Discussionmentioning
confidence: 99%
“…In the already K + -depolarized artery, histamine induces additional uptake of extracellular Ca ++ (Karaki and Weiss, 1980) and releases intracellularly bound Ca ++ from sites that are not sites of Ca ++ -sequestration (Deth and van Breeman, 1977), but does not further alter membrane potential (Suzuki and Casteels, 1979). The dependence of histamineinduced contraction on external [Ca ++ ] (Hudgins and Weiss, 1968;Watkins and Davidson, 1980) suggests that tonic histaminergic vasoconstriction (such as utilized here) is primarily the result of a voltage-independent increase in membrane permeability to external Ca ++ (Harder, 1980). Although the reactivity of blood vessels to histamine is highly variable (Vanhoutte 1978), the net systemic action of histamine is a vasodilation of the fine blood vessels, which is mediated primarily through H2-histaminergic receptors (cf Douglas, 1975;Levy, 1977).…”
mentioning
confidence: 88%