Calcium kinetics in the aorta of spontaneously hypertensive rats

Zsoter, T; Wolchinsky, C.; Henein, Nabil F.; Ho, Lee Kwang

doi:10.1093/cvr/11.4.353

Cited by 47 publications

(5 citation statements)

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“…Although the isolated SHR aorta is reported to be less calcium sensitive (Lederballe Pedersen, Mikkelsen & Andersson, 1978), other investigators (Noon, Rice & Baldessanni, 1978) found an increased tone in this preparation, which is calcium-dependent. In support of the findings of Noon et al, a greater plasma-membrane Ca-flux has been found in aorta from SHRs (Zsoter, Wolchinsky, Henein & Ho, 1977) while in subcellular fractions of SHR mesenteric arteries there is an increased plasma-membrane uptake of calcium (Wei, Janis & Daniel, 1976). These noradrenalinestimulated calcium-sensitivity differences are in contrast to the reports concerning calcium-sensitivity with potassium stimulation.…”

Section: Vascular Supersensitivity In the Shrsupporting

confidence: 69%

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

Mulvany

Nyborg

1980

British J Pharmacology

195

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1 We have measured the calcium sensitivity in response to noradrenaline stimulation and potassium depolarization of isolated segments of 100 to 200 gm mesenteric resistance vessels from spontaneously hypertensive (SHR) and control Wistar-Kyoto (WKY) rats. The rats were either young (4 wk) or adult (4 months), that is of ages before or after the SHRs had developed elevated blood pressure. Experiments were performed under conditions in which the effect of noradrenaline uptake by, and the potassium-induced noradrenaline release from, the nerve terminals in the vessel walls was eliminated. 2 The response of the SHR and WKY vessels to noradrenaline under conditions where only the extracellular calcium appeared to have been removed was similar. When subsequently stimulated maximally by noradrenaline, the calcium-sensitivity of the SHR vessels (Ca-ED50 -0.1 mM) was greater than that of the WKY vessels (Ca-EDs5 -0.2 mM). When depolarized by potassium, all vessels were less sensitive to calcium and there was little difference in the calcium sensitivity of SHR and WKY vessels in either age group (Ca-ED50 o 0.8 mM). 3 The results suggest that whereas the potassium (potential)-dependent calcium permeability of the SHR smooth muscle cell membrane is normal, the noradrenaline-induced calcium permeability is abnormally high. The presence of this abnormality in the vessels from the young SHRs suggests that it may be a factor involved in the aetiology of hypertension in the SHR.

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Section: Vascular Supersensitivity In the Shrsupporting

confidence: 69%

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

Mulvany

Nyborg

1980

British J Pharmacology

195

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“…This finding is in agreement with the results of life-time treatment with propranolol (in a similar dose) or timolol (Nishiyama et al, 1978). Other investigators also reported no blood pressure lowering effect of smaller doses of P-adrenoceptor blocking agents given alone (Scriabine et al, 1974;Uchiyama et al, 1977;Zsotkr & Wolchinsky, 1978). However, a definite dose dependency of propranolol regarding antihypertensive effect was reported by Kubo et al (1977).…”

Section: Influence Of Antihypertensive Treatment On Vascular Responsesupporting

confidence: 82%

“…45Ca efflux was not found to differ. In a similar study by Zsotkr et al (1977), the unstimulated uptake of 45C'a was found to be significantly smaller in hypertensive aortae and the initial efflux rates faster. Bhalla et al (1978) measured 45Ca influx in SHR aorta using a long post-incubation period in calciumfree medium containing La+++.…”

Section: Defective Membranal Transport Andor Defective Intracellular mentioning

confidence: 70%

Calcium Blockade as a Therapeutic Principle in Arterial Hypertension: Clinical aspects and experimental studies on isolated vessels from spontaneously hypertensive rats and normotensive man.

Pedersen¹

1981

Acta Pharmacologica et Toxicologica

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“…Several hypotheses have been proposed to explain this increase in sensitivity to involve a generalized increase in the contractility of the blood vessels or a reduced relaxation to vasodilators (Winquist & Bohr, 1983;Cohen & Berkowitz, 1976). Other studies have suggested that the increased sensitivity of hypertensive blood vessels results from an alteration in the regulation of calcium influx in vascular muscle (Shibata et al, 1975;Zsoter et al, 1977). The contractile machinery in muscles is activated by a rise in intracellular calcium.…”

Section: Introductionmentioning

confidence: 99%

Hepoxilins sensitize blood vessels to noradrenaline—stereospecificity of action

Laneuville

Couture

Pace-Asciak

1992

British J Pharmacology

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1 The vascular activity of two stereoisomers of hepoxilin A3 (HxA3) (8R and 8S) and of its glutathione conjugate, hepoxilin A3-C (HxA3-C) (8R and 8S), was investigated on rat helicoidal strips of thoracic aorta and longitudinal strips of portal vein.2 Neither of the hepoxilins tested had a direct effect on the tone of the aortic strip or on the spontaneous contractions of the portal vein. However, the noradrenaline (NA)-induced response of these vessels, as expressed by the dose required for half maximal contraction, (EC50) was greater in HxA3 (8S)-and HxA3-C (8R)-treated aorta. Increased frequency and strength of spontaneous contractions of the portal vein were detected at lower concentrations of NA in the presence of hepoxilins. 3 The threshold dose for both hepoxilins was 10-8M and their effect was not dose-related beyond 10-8m. The effect of hepoxilin appeared after a 45min incubation period and could be observed even if the compounds were washed out after 15 min. 4 Stereochemical specificity was observed. The 8S isomer of HxA3 was active in potentiating the NAinduced contraction of these vessels while the 8R isomer was inactive. In contrast, the 8R isomer of HxA3-C was active while the 8S isomer was inactive. In both tissues, HxA3 (8S) was more potent than its glutathione conjugate, HxA3-C (8R).5 In calcium-free buffer or in the presence of a calcium channel blocker (nifedipine 1 pM), no potentiation of NA-induced contraction by hepoxilins could be observed, suggesting the involvement of extracellular calcium in the actions of hepoxilins. 6 These experiments suggest that hepoxilins may be involved in the modulation of vascular tone and contractility.

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Calcium kinetics in the aorta of spontaneously hypertensive rats

Cited by 47 publications

References 0 publications

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

Calcium Blockade as a Therapeutic Principle in Arterial Hypertension: Clinical aspects and experimental studies on isolated vessels from spontaneously hypertensive rats and normotensive man.

Hepoxilins sensitize blood vessels to noradrenaline—stereospecificity of action

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