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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1989-6-8
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pubmed:abstractText |
Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0085-2538
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
35
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
717-36
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2540374-Adult,
pubmed-meshheading:2540374-Animals,
pubmed-meshheading:2540374-Calcium,
pubmed-meshheading:2540374-Calcium, Dietary,
pubmed-meshheading:2540374-Calcium Channels,
pubmed-meshheading:2540374-Humans,
pubmed-meshheading:2540374-Hypertension,
pubmed-meshheading:2540374-Male
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pubmed:year |
1989
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pubmed:articleTitle |
Calcium metabolism and hypertension.
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pubmed:affiliation |
Oregon Health Sciences University, Portland.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Case Reports,
Research Support, Non-U.S. Gov't
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