1986
DOI: 10.1161/01.hyp.8.8.694
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Hyperreactivity of platelets from spontaneously hypertensive rats. Role of external magnesium.

Abstract: Received February 5, 1985; accepted February 4, 1986. lease their granular content in a manner similar to that of nerve terminals. The aim of the present study was to determine whether platelet reactivity was altered in spontaneously hypertensive rats (SHR) and, if so, whether this alteration existed at the prehypertensive stage. In addition, we compared the functional response of platelets from hypertensive and control Wistar-Kyoto rats (WKY) to different external calcium concentrations to define the mecha… Show more

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Cited by 42 publications
(14 citation statements)
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“…Magnesium deficiency has been associated with CSD (Strong et al 2002), neurotransmitter release (Coan and Collingridge 1985), platelet aggregation (Baudouin-Legros et al 1986), and vasoconstriction Altura 1982, 1989) Substance P is released as a result of magnesium deficiency, which is hypothesized to act on sensory fibers and produce headache pain (Innerarity 2000) External magnesium may help to diminish various aspects of neurogenic inflammation. It is involved in the control of NMDA glutamate receptors, which play an important role in pain transmission within the nervous system (Foster and Fagg 1987) and in regulation of cerebral blood flow (Huang et al 1994).…”
Section: Pathophysiologymentioning
confidence: 99%
“…Magnesium deficiency has been associated with CSD (Strong et al 2002), neurotransmitter release (Coan and Collingridge 1985), platelet aggregation (Baudouin-Legros et al 1986), and vasoconstriction Altura 1982, 1989) Substance P is released as a result of magnesium deficiency, which is hypothesized to act on sensory fibers and produce headache pain (Innerarity 2000) External magnesium may help to diminish various aspects of neurogenic inflammation. It is involved in the control of NMDA glutamate receptors, which play an important role in pain transmission within the nervous system (Foster and Fagg 1987) and in regulation of cerebral blood flow (Huang et al 1994).…”
Section: Pathophysiologymentioning
confidence: 99%
“…1,2 Based on previous studies showing evidence of Mg reduction in patients with migraine, Mg deficiency may play an important role in migraine biogenesis. [18][19][20] Reduced Mg levels enhance the sensitivity of the N -methyl-Daspartate (NMDA) receptors to glutamate, facilitat-ing the development of cortical spreading depression. [18][19][20] Reduced Mg levels enhance the sensitivity of the N -methyl-Daspartate (NMDA) receptors to glutamate, facilitat-ing the development of cortical spreading depression.…”
mentioning
confidence: 99%
“…First, familial hemiplegic migraine could be a Ca channelopathy and one could hypothesize that, acting as a physiological antagonist of Ca, Mg might exert a beneficial effect in more prevalent forms of migraine. [45][46][47][48][49][50] We recommend longer, larger trials using higher but still tolerable doses of well-absorbed Mg salts in carefully chosen study populations to definitively establish the place of Mg therapy in migraine prophylaxis. [40][41][42] This process may be linked to cortical spreading depression of Leão triggered by stimulation of N -methyl-D -aspartate (NMDA) receptors.…”
Section: June 2003mentioning
confidence: 99%