Calcium Metabolism in Experimental Hypertension
Calcium Metabolism in Experimental Hypertension
复制标题
实验性高血压中的钙代谢
DOI：
--
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
D. McCarron
中科院分区：
文献类型：
--
作者：
E. Young;R. Bukoski;D. McCarron
Conclusion Clearly, Ca2+ metabolism is altered in hypertension at both the whole animal and cellular level. Furthermore, dietary Ca2+ deficiency is associated with human hypertension at the epidemiologic level and oral Ca2+ supplementation lowers blood pressure in human and experimental hypertension. In this review, we have presented the integrated view that a constellation of systemic abnormalities of Ca2+ metabolism in hypertension results in inefficient Ca2+ conservation and relative Ca2+ deficiency. Furthermore, the cellular findings in hypertension suggest increased cell membrane Ca2+ permeability and a compromised ability of the cell to remove or sequester intracellular Ca2+. Paradoxically this leads to increased intracellular free Ca2+ stores in the face of reduced extracellular Ca2+. Unfortunately most of the whole animal and cellular work has been carried out using different tissues. Nonetheless, it seems reasonable to hypothesize that abnormal Ca2+ handling at the cellular level is ultimately reflected at the organ and whole animal level so that alterations in vascular smooth muscle, intestine, kidney, erythrocytes, and so on are due to the same underlying defect manifested in many cell lines. The underlying defect may involve the cell membrane Ca2+-ATPase (68), an intrinsic membrane binding protein (114), a cell membrane Ca2+ channel, or perhaps some other process. If an underlying cellular defect in Ca2+ metabolism exists in some forms of hypertension, then what is the link with elevated blood pressure? While altered Ca2+ metabolism in hypertension may be an epiphenomenon of some other metabolic process that is primarily responsible for the elevated blood pressure, a more central role for altered Ca2+ metabolism in hypertension is suggested by the myriad of defects that have been reported. However, the issue will remain unsettled until the underlying bases for disrupted calcium and vascular homeostasis in hypertension are found. Understanding of calcium metabolism and blood pressure regulation in hypertension, whether as shared or separate mechanisms, should prove to be a challenging but productive area of future research.
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自发性高血压大鼠体内对 1,25(OH)2D3 的反应。
影响因子：
19.6
作者：
Gafter,U;Eby,B;Martin,C;Lau,K
通讯作者：
Lau,K
Ca 流过自发性高血压大鼠的十二指肠和结肠：1,25(OH)2D3 的影响。
DOI：
10.1152/ajprenal.1986.251.2.f278
发表时间：
1986
期刊：
The American journal of physiology
影响因子：
--
作者：
Gafter,U;Kathpalia,S;Zikos,D;Lau,K
通讯作者：
Lau,K
DOI：
10.1093/ajcn/38.3.457
发表时间：
1983-09
期刊：
The American journal of clinical nutrition
影响因子：
--
作者：
S. Ackley;E. Barrett-Connor;Lucina Suarez
通讯作者：
S. Ackley;E. Barrett-Connor;Lucina Suarez
影响因子：
4.9
作者：
S. Umemura;D. Smyth;M. Nicar;J. Rapp;W. Pettinger
通讯作者：
S. Umemura;D. Smyth;M. Nicar;J. Rapp;W. Pettinger
自发性高血压大鼠组织中整合膜钙结合蛋白（IMCAL）含量降低。
DOI：
10.1073/pnas.83.4.1097
发表时间：
1986
影响因子：
11.1
作者：
Kowarski,S;Cowen,LA;Schachter,D
通讯作者：
Schachter,D