Parallel Reduction of Calcium-Influx-Dependent Vasoconstriction and Platelet-Free Calcium Concentration with Calcium Entry and ??-Adrenoceptor Blockade

Bolli, Peter; Erné, Paul; Ul, Hulthén; Ritz, R; Kiowski, Wolfgang; Bh, Ji; Fr, Bühler

doi:10.1097/00005344-198400067-00013

Cited by 37 publications

(6 citation statements)

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“…1 " 3 This derangement is due to structural differences between normotensive and hypertensive subjects, 4 but also entails functional components. 5 As the force-generating bridging between actin and myosin depends on changes of intracellular calcium activity (calcium free-ion concentration) and hence transmembranous calcium movements, modulations of transmembranous calcium influx and intracellular cal-cium activity, (Ca 2+ )i7 have a pivotal role in determining vasoconstriction. Therefore, mechanisms that lead to an increase in (Ca 2+ )i through these processes cause vasoconstriction.…”

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confidence: 99%

Cellular Calcium Regulation in Hypertension

Hermsmeyer

Erné

1989

American Journal of Hypertension

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In vascular muscle cells, two distinct types of functionally important calcium (Ca 2+ ) channels, called transient (T) and sustained (L), are differentiated by dihydropyridine calcium antagonists (CaA). We studied the ratio of T/L Ca 2+ However, these studies do not determine whether similar alterations are operative in vascular muscle cells and, if so, whether they are causally implicated or a consequence of elevated blood pressure.To define vascular muscle mechanisms which are altered in an animal model of hypertension prior to the development of elevated blood pressure, studies were

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confidence: 99%

Cellular Calcium Regulation in Hypertension

Hermsmeyer

Erné

1989

American Journal of Hypertension

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“…In platelets, cytosolic [Ca 2+ ] was found to be related to blood pressure (12,13) and to the forearm vascular resistance (14). A parallel reduction of Ca 2+ influx-dependent vasoconstriction and of platelet Ca 2+ concentration with Ca 2+ entry and ␤-adrenoceptor blockade has been previously observed (15). The increased cytosolic Ca 2+ in platelets could thus reflect the increased cytosolic Ca 2+ in smooth muscle cells and vascular tone, although no direct relationship between platelets and vascular smooth muscle cells with respect to Ca 2+ concentration or metabolism has been reported.…”

Section: Introductionmentioning

confidence: 69%

Relations of Platelet Ca2+ Handling and Membrane Microviscosity to Vascular Tone and Restenosis after Angioplasty in Human Coronary Artery

Kh²,

Brunet³

et al. 1998

Thromb Haemost

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SummaryThis study was designed to assess whether platelet Ca2+ handling or membrane microviscosity could be considered as indexes of vascular tone, or could help to predict an increased risk of restenosis after coronary angioplasty. Vascular tone was quantified in 21 patients with stable angina by the vasodilator response to sin-1 intracoronary injection in the reference coronary segment and by the importance of the acute recoil after angioplasty in the narrowed segment. The degree of restenosis was quantified by coronary angiography 6 months later.Individual values of relative sin-1-induced changes in the reference coronary diameter were positively correlated with cytosolic Ca2+ concentration in unstimulated platelets, irrespective of the extracellular Ca2+ concentration (p <0.01). This relationship was also observed with the thrombin-evoked Ca2+ changes, measured in the absence of a Ca2+ influx (p = 0.01). No relationship was found between sin-1-induced coronary changes and membrane microviscosity evaluated by TMADPH and DPH anisotropies or platelet volume, or between degree of acute recoil and platelet characteristics.In conclusion, platelet Ca2+ reflects the vasodilating efficacy in response to sin-1, but cannot help to predict restenosis after coronary angioplasty.

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“…These results were consistent with findings in earlier reports of altered calcium metabolism due to chronic alcohol consumption in rats (7-9, 23). We chose to investigate platelets because they exhibit abnormalities in calcium handling similar to those described in vascular smooth muscle cells, which share many common intracellular features with platelets including a calcium-dependent concentrationcoupling process (24,25).…”

Section: Discussionmentioning

confidence: 99%

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

Harada¹,

Kitazaki²,

Tsujino

et al. 2000

Hypertens Res

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YOKOYAMATaurine is known to lower blood pressure in essential hypertension and some experimental hypertensive models. Taurine has also been reported to activate aldehyde dehydrogenase and to inhibit the elevation of plasma acetaldehyde concentration after ethanol intake. Because acetaldehyde, the first metabolite of ethanol, is suspected to be responsible for many adverse effects of alcohol consumption, we examined the effect of taurine supplementation on ethanol-induced hypertension and abnormalities in the intracellular cation metabolism in Witar-Kyoto rats. In Study 1, systolic blood pressure and intraplatelet free calcium were significantly higher in rats who received 15% ethanol in drinking water than in control rats. Oral taurine supplementation (1% taurine and 15% ethanol in drinking water) completely prevented the development of ethanol-induced hypertension. Intraerythrocyte sodium and intraplatelet free calcium were significantly decreased in taurine-supplemented rats as compared with rats who received 15% ethanol only. In Study 2, hemoglobin-associated acetaldehyde (HbAA) was measured as a marker of protein-bound acetaldehyde. HbAA was significantly elevated in rats who received 5% ethanol in drinking water as compared with control rats. Taurine supplementation (1% taurine and 5% ethanol in drinking water) significantly decreased HbAA. Our findings suggest that the oral supplementation of taurine prevents ethanol-induced hypertension by decreasing protein bound acetaldehyde and altering the cation handling by the membrane. (Hypertens Res 2000; 23: 277-284)

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Parallel Reduction of Calcium-Influx-Dependent Vasoconstriction and Platelet-Free Calcium Concentration with Calcium Entry and ??-Adrenoceptor Blockade

Cited by 37 publications

References 0 publications

Cellular Calcium Regulation in Hypertension

Cellular Calcium Regulation in Hypertension

Relations of Platelet Ca2+ Handling and Membrane Microviscosity to Vascular Tone and Restenosis after Angioplasty in Human Coronary Artery

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

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