Effect of prostacyclin on platelet intracellular free calcium concentration of hypertensive and normotensive humans

Hiroaki Komura; Richard D. Bukoski; Njeri Karanja; Cynthia D. Morris; Tetsuji Shingu; David A. McCarron

doi:10.1093/ajh/6.9.730

Effect of prostacyclin on platelet intracellular free calcium concentration of hypertensive and normotensive humans

Hiroaki Komura, Richard D. Bukoski, Njeri Karanja, Cynthia D. Morris, Tetsuji Shingu, David A. McCarron

Medical Informatics and Clinical Epidemiology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Platelet intracellular free calcium concentration ([Ca²⁺]j) has been reported to be increased in essential hypertensive patients (EHT) as compared with normotensive controls (NT). Prostacyclin (PGI₂), which influences cellular Ca²⁺, has been reported to be reduced in EHT. This study tested the hypothesis that the resting level of platelet [Ca²⁺]j in humans is influenced by PGI₂. We also investigated the role of PGI₂ in regulating platelet [Ca²⁺]_iof 28 EHT subjects compared to 28 NT controls. Platelet [Ca²⁺] was measured using the fluorescent Ca²⁺ probe fura-2 under control conditions and a 10-min preincubation with PGI₂. Simultaneous measurement of platelet cyclic-adenosine 3':5'- monophosphate (cAMP) was performed by radioimmunoassay. The resting level of platelet [Ca²⁺]_iwas significantly higher in EHT than in NT (32.7 ±1.4 v 28.3 ± 0.9 nmol/L; P <.01). PGI₂ from 30 nM to 1//mol/L lowered the resting level of platelet [Ca² in a dose-dependent manner (EHT —22.2 ± 2.4, NT —22.9 ± 2.3%, 1/mol/L PGI₂); however, no significant difference in platelet [Ca²⁺]i was observed between NT and EHT. While prostacyclin induced a transient rise in platelet cAMP, the magnitude of PGI₂-induced cAMP level was similar between the two groups. These results do not support the hypothesis that endogenous PGI₂ activity contributes to the increased level of platelet [Ca²⁺]i in EHT, although PGI₂ incubation lowered the resting level of platelet [Ca²⁺]j.

Original language	English (US)
Pages (from-to)	730-735
Number of pages	6
Journal	American Journal of Hypertension
Volume	6
Issue number	9
DOIs	https://doi.org/10.1093/ajh/6.9.730
State	Published - Sep 1993

Keywords

CAMP
Calcium
Essential hypertension
Platelet
Prostacyclin

ASJC Scopus subject areas

Internal Medicine

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10.1093/ajh/6.9.730

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@article{cb732fe80a0c4a1688f78646f4613257,

title = "Effect of prostacyclin on platelet intracellular free calcium concentration of hypertensive and normotensive humans",

abstract = "Platelet intracellular free calcium concentration ([Ca2+]j) has been reported to be increased in essential hypertensive patients (EHT) as compared with normotensive controls (NT). Prostacyclin (PGI2), which influences cellular Ca2+, has been reported to be reduced in EHT. This study tested the hypothesis that the resting level of platelet [Ca2+]j in humans is influenced by PGI2. We also investigated the role of PGI2 in regulating platelet [Ca2+]iof 28 EHT subjects compared to 28 NT controls. Platelet [Ca2+] was measured using the fluorescent Ca2+ probe fura-2 under control conditions and a 10-min preincubation with PGI2. Simultaneous measurement of platelet cyclic-adenosine 3':5'- monophosphate (cAMP) was performed by radioimmunoassay. The resting level of platelet [Ca2+]iwas significantly higher in EHT than in NT (32.7 ±1.4 v 28.3 ± 0.9 nmol/L; P <.01). PGI2 from 30 nM to 1//mol/L lowered the resting level of platelet [Ca2 in a dose-dependent manner (EHT —22.2 ± 2.4, NT —22.9 ± 2.3%, 1/mol/L PGI2); however, no significant difference in platelet [Ca2+]i was observed between NT and EHT. While prostacyclin induced a transient rise in platelet cAMP, the magnitude of PGI2-induced cAMP level was similar between the two groups. These results do not support the hypothesis that endogenous PGI2 activity contributes to the increased level of platelet [Ca2+]i in EHT, although PGI2 incubation lowered the resting level of platelet [Ca2+]j.",

keywords = "CAMP, Calcium, Essential hypertension, Platelet, Prostacyclin",

author = "Hiroaki Komura and Bukoski, {Richard D.} and Njeri Karanja and Morris, {Cynthia D.} and Tetsuji Shingu and McCarron, {David A.}",

note = "Funding Information: The authors are grateful to Dr. Tetsuya Oshima of Hiroshima University for his advice. We would like to thank Gwen Hanson for the recruitment of patients, Scott Holcomb for the statistical analysis, and Jerilyn Prescott for excellent technical assistance. This work was supported in part by Clinical Nutrition Research Unit DK 40566-04, and grants from the National Dairy Promotion and Research Board, the Salt Institute, and Campbell's Foundation.",

year = "1993",

month = sep,

doi = "10.1093/ajh/6.9.730",

language = "English (US)",

volume = "6",

pages = "730--735",

journal = "American Journal of Hypertension",

issn = "0895-7061",

publisher = "Oxford University Press",

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T1 - Effect of prostacyclin on platelet intracellular free calcium concentration of hypertensive and normotensive humans

AU - Komura, Hiroaki

AU - Bukoski, Richard D.

AU - Karanja, Njeri

AU - Morris, Cynthia D.

AU - Shingu, Tetsuji

AU - McCarron, David A.

N1 - Funding Information: The authors are grateful to Dr. Tetsuya Oshima of Hiroshima University for his advice. We would like to thank Gwen Hanson for the recruitment of patients, Scott Holcomb for the statistical analysis, and Jerilyn Prescott for excellent technical assistance. This work was supported in part by Clinical Nutrition Research Unit DK 40566-04, and grants from the National Dairy Promotion and Research Board, the Salt Institute, and Campbell's Foundation.

PY - 1993/9

Y1 - 1993/9

N2 - Platelet intracellular free calcium concentration ([Ca2+]j) has been reported to be increased in essential hypertensive patients (EHT) as compared with normotensive controls (NT). Prostacyclin (PGI2), which influences cellular Ca2+, has been reported to be reduced in EHT. This study tested the hypothesis that the resting level of platelet [Ca2+]j in humans is influenced by PGI2. We also investigated the role of PGI2 in regulating platelet [Ca2+]iof 28 EHT subjects compared to 28 NT controls. Platelet [Ca2+] was measured using the fluorescent Ca2+ probe fura-2 under control conditions and a 10-min preincubation with PGI2. Simultaneous measurement of platelet cyclic-adenosine 3':5'- monophosphate (cAMP) was performed by radioimmunoassay. The resting level of platelet [Ca2+]iwas significantly higher in EHT than in NT (32.7 ±1.4 v 28.3 ± 0.9 nmol/L; P <.01). PGI2 from 30 nM to 1//mol/L lowered the resting level of platelet [Ca2 in a dose-dependent manner (EHT —22.2 ± 2.4, NT —22.9 ± 2.3%, 1/mol/L PGI2); however, no significant difference in platelet [Ca2+]i was observed between NT and EHT. While prostacyclin induced a transient rise in platelet cAMP, the magnitude of PGI2-induced cAMP level was similar between the two groups. These results do not support the hypothesis that endogenous PGI2 activity contributes to the increased level of platelet [Ca2+]i in EHT, although PGI2 incubation lowered the resting level of platelet [Ca2+]j.

AB - Platelet intracellular free calcium concentration ([Ca2+]j) has been reported to be increased in essential hypertensive patients (EHT) as compared with normotensive controls (NT). Prostacyclin (PGI2), which influences cellular Ca2+, has been reported to be reduced in EHT. This study tested the hypothesis that the resting level of platelet [Ca2+]j in humans is influenced by PGI2. We also investigated the role of PGI2 in regulating platelet [Ca2+]iof 28 EHT subjects compared to 28 NT controls. Platelet [Ca2+] was measured using the fluorescent Ca2+ probe fura-2 under control conditions and a 10-min preincubation with PGI2. Simultaneous measurement of platelet cyclic-adenosine 3':5'- monophosphate (cAMP) was performed by radioimmunoassay. The resting level of platelet [Ca2+]iwas significantly higher in EHT than in NT (32.7 ±1.4 v 28.3 ± 0.9 nmol/L; P <.01). PGI2 from 30 nM to 1//mol/L lowered the resting level of platelet [Ca2 in a dose-dependent manner (EHT —22.2 ± 2.4, NT —22.9 ± 2.3%, 1/mol/L PGI2); however, no significant difference in platelet [Ca2+]i was observed between NT and EHT. While prostacyclin induced a transient rise in platelet cAMP, the magnitude of PGI2-induced cAMP level was similar between the two groups. These results do not support the hypothesis that endogenous PGI2 activity contributes to the increased level of platelet [Ca2+]i in EHT, although PGI2 incubation lowered the resting level of platelet [Ca2+]j.

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KW - Essential hypertension

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KW - Prostacyclin

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Effect of prostacyclin on platelet intracellular free calcium concentration of hypertensive and normotensive humans

Abstract

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