Dietary NaCl Loading Increases Platelet Ca2+ Discharge Capacity in Salt Resistant Essential Hypertension

Watanabe Mitsuaki

Hiroshima Journal of Medical Sciences

[PISSN] 0018-2052

[EISSN] 2433-7668

[NCID] AA00664312

To clarify the relationship between cellular Ca2+ handling and salt sensitivity, we evaluated cytosolic free Ca2+ ([Ca2+]i) in fura-2 loaded platelets isolated from 20 inpatients with essential hypertension. They were placed on a low sodium diet (50 mmol/day) for one week, followed by one week on a high sodium diet (340 mmol/day). They were classified into salt-sensitive (SS, n=8) or salt-resistant (SR, n=12) based on changes in the mean blood pressure. During the low salt diet, basal [Ca2+]i, thrombin-evoked maximal Ca2+ responses, irrespective of the presence of 1 mM extracellular Ca2+, and ionomycin-sensitive intracellular Ca2+ discharge capacity were similar in salt-sensitive and salt-resistant patients. Platelet basal [Ca2+]i were increased in both groups by salt loading (SS, from 22.0±1.3 to 27.2±1.9 nM, p<0.01; SR, from 20.1±0.8 to 24.4±1.3 nM, p<0.05). The thrombin-evoked maximal Ca2+ responses both in the presence and absence of extracellular Ca2+ were unchanged by high salt intake. The rate constant of decline in Ca2+ after the peak response to thrombin was larger in SR than that in SS during the high salt diet period (SS, 0.004 ± 0.001 sec-1; SR, 0.043 ± 0.014 sec-1, p<0.05). The intracellular Ca2+ discharge capacity was increased by excessive salt intake in the salt-resistant patients but was unchanged in the salt-sensitive patients (SS, from 658. l ± 52.8 to 639.6 ± 91.9 nM; SR, from 690.8 ± 65.1 to 803.3 ± 65.1 nM, p<0.05). An increased intracellular Ca2+ discharge capacity may play, at least in part, a significant role in preventing the elevation of blood pressure after salt loading in salt-resistant patients with essential hypertension.

Salt sensitivity

Calcium

Platelet

Essential hypertension

Medical sciences [ 490 ]

eng

Hiroshima University Medical Press

[ISSN] 0018-2052

[NCID] AA00664312