Cytosolic free calcium of aorta in hypertensive rats. Chronic inhibition of angiotensin converting enzyme.

Sada, Toshio; Koike, Hiroyuki; Ikeda, Masahiro; Sato, Koichi; Ozaki, Hiroshi; Karaki, Hideaki

doi:10.1161/01.hyp.16.3.245

Cited by 74 publications

(28 citation statements)

References 33 publications

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“…The increased cellular Ca2" uptake or content in the resting state has been demonstrated in aortae from SHR (van Breemen et al, 1986;Jelicks & Gupta, 1990;Sada et al, 1990 (Asano et al, 1986). Although no measurements of the resting membrane potential are available in the present study, membrane depolarization in SHR arteries has been demonstrated in the mesenteric artery (Fujii et al, 1992), the tail artery (Cheung, 1984), and the aorta (Tomobe et al, 1991 Small conductance KCa channels might be activated in the resting state of SHR arteries by the increased cellular Ca2+ uptake.…”

Section: Discussionmentioning

confidence: 94%

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Asano

Masuzawa-Ito

Matsuda

1993

British J Pharmacology

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1 To determine the possible role of Ca2"-activated K+ (Kca) channels in the regulation of resting tone of arteries from spontaneously hypertensive rats (SHR), the effects of agents which interact with these channels on tension and 16Rb efflux were compared in endothelium-denuded strips of carotid, femoral and mesenteric arteries from SHR and normotensive Wistar-Kyoto rats (WKY). 2 Strips of carotid, femoral and mesenteric arteries from SHR exhibited a myogenic tone; that is, the resting tone decreased when either the Krebs solution was changed to a 0-Ca2+ solution or 10-7M nifedipine was added.3 The addition of charybdotoxin (ChTX, I0-'-I0-M), a blocker of large conductance Kca channels, to the resting strips of these arteries produced a concentration-dependent contraction, which was significantly greater in SHR than in WKY. Relatively low concentrations of tetraethylammonium (0.05-5 mM) produced a concentration-dependent contraction which was similar to the ChTX-induced contraction in these strips. 4 The ChTX-induced contractions in SHR were greatly attenuated by 10-7 M nifedipine and by 3 X 10-6 M cromakalim, a K+ channel opener. Cromakalim alone abolished the myogenic tone in SHR. 5 The addition of apamin (a blocker of small conductance Kca channels, up to 10-6 M), or of glibenclamide (a blocker of ATP-sensitive K+ channels, up to 5 x 10-6 M ), to the resting strips failed to produce a contraction.6 In resting strips of carotid, femoral and mesenteric arteries preloaded with 86Rb, the basal 86Rb efflux rate constants were significantly greater in SHR than in WKY. The addition of 10-7 M nifedipine to the resting strips decreased the basal 86Rb efflux rate constants only in SHR. 7 The cellular Ca2+ uptake in the resting state of carotid and femoral arteries from SHR was significantly increased when compared to WKY, and this increase in SHR was significantly reduced by 10-7 M nifedipine. 8 These results suggest that the ChTX-sensitive KCa channels were highly activated to regulate the myogenic tone in the resting state of carotid, femoral and mesenteric arteries from SHR. The increased Kca channel functions in SHR arteries appeared to be secondary to the increased Ca2' influx via L-type voltage-dependent Ca2+ channels in the resting state of these arteries.

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Section: Discussionmentioning

confidence: 94%

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Asano

Masuzawa-Ito

Matsuda

1993

British J Pharmacology

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“…Endothelium-removed preparations of large arteries from spontaneously hypertensive rats have been shown to develop spontaneous active tone (Noon et al, 1978;Sada et al, 1990). The present experiments indicated that the tone is sensitive to either extracellular Ca 2+ or to Ca…”

Section: Discussionmentioning

confidence: 99%

“…Large arteries of hypertensive rats have been shown to develop spontaneous tonic myogenic contractions (Noon et al, 1978;Sada et al, 1990). We have reported that the endotheliumCorrespondence to: K. Shimamura, Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Health Science University of Hokkaido, Kanazawa 1757, Ishikari-Tobetsu, Hokkaido 061-0293, Japan Phone: +81-1332-3-1211 ext.3160 Fax: +81-1332-3-1669 e-mail: shimamu@hoku-iryo-u.ac.jp removed carotid artery of stroke-prone spontaneously hypertensive rats (SHRSP) contracts spontaneously with an increase in intracellular free Ca 2+ concentration (Sekiguchi et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Effects of Flufenamic Acid on Smooth Muscle of the Carotid Artery Isolated from Spontaneously Hypertensive Rats.

Shimamura

Zhou

Ito

et al. 2002

J. Smooth Muscle Res.

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“…- 39 The hyperactivity of L-type Ca 2+ channels in resting SHR VSMCs may be caused by a partial depolarization of the smooth muscle cell sarcolemma, as described previously for SHRs. 40 The increased basal Ca 2+ uptake of VSMCs could contribute toward both the increased calcium-dependent spontaneous tone and enhanced calcium-induced contraction observed in aortic strips from SHRs.…”

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confidence: 85%

Vascular smooth muscle cell calcium fluxes. Regulation by angiotensin II and lipoproteins.

et al. 1993

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This study examined 4SCa uptake, 45 Ca efflux, and the distribution of exchangeable 4SCa in confluent, quiescent cultures of aortic smooth muscle cells (VSMCs) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). These parameters were investigated under basal conditions and after addition of angiotensin II (Ang II) and low (LDL) (Ang II) 1 is an important regulator / \ not only of vascular smooth muscle contraction A. A . but also of vascular smooth muscle cell (VSMC) growth (see References 1 and 2 for reviews). In hypertension, both the functional and structural integrity of vascular smooth muscle are deranged, 12 thus invoking an essential involvement of Ang II in the pathophysiology of hypertension. This is supported by observations that angiotensin converting enzyme inhibitors effectively lower blood pressure 3 and also prevent myointimal proliferation after vascular injury. 4 Hypertension greatly increases the frequency of atherosclerotic cardiovascular sequelae, and lipoproteins greatly affect the impact of hypertension on the pace of atherogenesis (see References 5 and 6 for reviews). The two diseases are closely linked with respect to predisposing risk factors, clinical manifestations, and vascular/cellular pathobiology; thus, the fundamental role of lipoproteins in the atherosclerotic process suggests that they may also be involved in the pathophysiology of hyper- tension. 5-6 Evidence is accumulating to indicate that low density lipoprotein (LDL) and high density lipoprotein (HDL) can influence smooth muscle cell processes that are distinct from those related to cholesterol homeostasis per se, such as growth-related metabolic events, cell morphology, and proliferation and contractile processes (reviewed in Reference 7).Calcium is a pivotal signaling molecule in the regulation of smooth muscle structure and function, and the hypothesis on the involvement of abnormalities of intracellular calcium handling in the pathophysiology of hypertension is based on the following principal observations.

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Cytosolic free calcium of aorta in hypertensive rats. Chronic inhibition of angiotensin converting enzyme.

Cited by 74 publications

References 33 publications

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Effects of Flufenamic Acid on Smooth Muscle of the Carotid Artery Isolated from Spontaneously Hypertensive Rats.

Vascular smooth muscle cell calcium fluxes. Regulation by angiotensin II and lipoproteins.

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Cytosolic free calcium of aorta in hypertensive rats. Chronic inhibition of angiotensin converting enzyme.

Cited by 74 publications

References 33 publications

Charybdotoxin‐sensitive K+ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K+ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Effects of Flufenamic Acid on Smooth Muscle of the Carotid Artery Isolated from Spontaneously Hypertensive Rats.

Vascular smooth muscle cell calcium fluxes. Regulation by angiotensin II and lipoproteins.

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Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats