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      Reduction in extracellular Ca 2+ attenuates endothelium-dependent relaxation more than nitroprusside-induced relaxation


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          To quantitatively assess the effect of lowering external Ca 2+ ([Ca 2+] o) on both endothelium-dependent and -independent relaxations in rabbit aorta.


          Isometric contractions and relaxations of isolated aortae were recorded. When assessing the effect of reduced [Ca 2+] o on relaxations, the normal [Ca 2+] o solution was substituted with one of the reduced [Ca 2+] o solutions for one aorta, while a paired aorta was replenished with normal [Ca 2+] o solution.


          The extent of acetylcholine (ACh)-induced relaxation, which is dependent on an intact endothelium, is time-dependent, and inversely related to [Ca 2+] o in a range of 0.02–2 mmol/L. ACh-induced relaxations were not significantly altered by the magnitude of the precontraction induced by PGF . Nitroprusside-induced relaxations, which are independent of the endothelium, are also attenuated by reduced [Ca 2+] o. Relaxant responses to ACh were significantly more susceptible to reduced [Ca 2+] o than nitroprusside-induced relaxations. A maximally effective relaxing concentration of D600, an L-type Ca channel blocker methoxyverapamil, (10 −5 mol/L) attenuated ACh-induced relaxations, whereas nitroprusside-induced relaxations were unaffected by D600.


          Thus, endothelium-dependent relaxation is more dependent on [Ca 2+] o than endothelium-independent relaxation, and it seems likely that [Ca 2+] o plays an important role not only in contractile processes, but also in relaxant processes as well.

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          Most cited references31

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          Role of endothelium in responses of vascular smooth muscle.

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            Acetylcholine-induced endothelium-dependent contractions in the SHR aorta: the Janus face of prostacyclin.

            In the spontaneously hypertensive rat (SHR) and aging Wistar-Kyoto rats (WKY), acetylcholine releases an endothelium-derived contracting factor (EDCF) produced by endothelial cyclooxygenase-1, which stimulates thromboxane A2 receptors (TP receptors) on vascular smooth muscle. The purpose of the present study was to identify this EDCF by measuring changes in isometric tension and the release of various prostaglandins by acetylcholine. In isolated aortic rings of SHR, U 46619, prostaglandin (PG) H2, PGF2alpha, PGE2, PGD2, prostacyclin (PGI2) and 8-isoprostane, all activate TP receptors of the vascular smooth muscle to produce a contraction (U 46619>8-isoprostane=PGF2alpha=PGH2>PGE2=PGD2>PGI2). The contractions produced by PGH2 and PGI2 were fast and transient, mimicking endothelium-dependent contractions. PGI2 did not relax isolated aortic rings of WKY and SHR. Acetylcholine evoked the endothelium-dependent release of thromboxane A2, PGF2alpha, PGE2, PGI2 and most likely PGH2 (PGI2>PGF2alpha>or=PGE2>TXA2>8-isoprostane, PGD2). Dazoxiben abolished the production of thromboxane A2, but did not influence the endothelium-dependent contractions to acetylcholine. The release of PGI2 was significantly larger in the aorta of SHR than in WKY, and the former was more sensitive to the contractile effect of PGI2 than the latter. The inhibition of PGI-synthase was associated with an increase in PGH2 spillover and the enhancement of acetylcholine-induced endothelium-dependent contractions. Thus, in the aorta of SHR and aging WKY, the endothelium-dependent contractions elicited by acetylcholine most likely involve the release of PGI2 with a concomitant contribution of PGH2.
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              Magnesium deficiency produces spasms of coronary arteries: relationship to etiology of sudden death ischemic heart disease.

              Isolated coronary arteries from dogs were incubated in Krebs-Ringer bicarbonate isolation and exposed to normal, high, and low concentrations of magnesium in the medium. Sudden withdrawal of magnesium from the medium increased whereas high concentrations of magnesium decreased the basal tension of the arteries. The absence of magnesium in the medium significantly potentiated the contractile responses of both small and large coronary arteries to norepinephrine, acetylcholine, serotonin, angiotensin, and potassium. These data support the hypothesis that magnesium deficiency, associated with sudden death ischemic heart disease, produces coronary arterial spasm.

                Author and article information

                Acta Pharmacol Sin
                Acta Pharmacol. Sin
                Acta Pharmacologica Sinica
                Nature Publishing Group
                January 2010
                16 November 2009
                : 31
                : 1
                : 19-26
                [1 ]Department of Medical Pharmacology and Toxicology, and Microcirculation Research Institute, College of Medicine, Texas A&M University, College Station , Texas 77843–1114, USA
                Author notes
                [* ]Faculty of Pharmaceutical Sciences, Ohu University , 31-1 Tomitacho-Misumido Koriyama 963-8611, Japan E-mail s-hayashi@ 123456pha.ohu-u.ac.jp
                Copyright © 2010 CPS and SIMM
                : 20 August 2009
                : 10 October 2009
                Original Article

                Pharmacology & Pharmaceutical medicine
                calcium,relaxation,vascular smooth muscle,aorta,endothelium,nitroprusside,d600


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