rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
3
|
pubmed:dateCreated |
1986-3-26
|
pubmed:abstractText |
A Ca2+-sensitive electrode was used to study net Ca2+-flux changes induced by the administration of phenylephrine, vasopressin and angiotensin to the perfused rat liver. The studies reveal that, although the Ca2+ responses induced by vasopressin and angiotensin are similar, they are quite different from the Ca2+ fluxes induced by phenylephrine. The administration of phenylephrine is accompanied by a stimulation of a net amount of Ca2+ efflux (140 nmol/g of liver). A re-uptake of a similar amount of Ca2+ occurs only after the hormone is removed. In contrast, the administration of vasopressin or angiotensin to livers perfused with 1.3 mM-Ca2+ induces the release of a relatively small amount of Ca2+ (approx. 40 nmol/g of liver) during the first 60 s. This is followed by a much larger amount of Ca2+ uptake (70-140 nmol/g of liver) after 1-2.5 min of hormone administration, and a slow efflux or loss of a similar amount of Ca2+ over a period of 6-8 min. At lower concentrations of perfusate Ca2+ (less than 600 microM) these hormones induce only a net efflux of the ion. These results suggest that at physiological concentrations of extracellular Ca2+ the mechanism by which alpha-adrenergic agonists mobilize cellular Ca2+ is different from that involving vasopressin and angiotensin. It seems that the hormones may have quite diverse effects on Ca2+ transport across the plasma membrane and perhaps organellar membranes in liver.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-2579567,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-3979569,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6087800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6092329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6095092,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6123310,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6131669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6134732,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6136270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6139276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6146314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6149742,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6150731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6239615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6269923,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6300115,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6320911,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6325442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6325926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6328320,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6333869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6413866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6430266,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6607924,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6610417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6693408,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6743272,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-6743279,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-7030320,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-7142184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-7264996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/4091828-807211
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0264-6021
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
232
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
911-7
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:4091828-Angiotensin II,
pubmed-meshheading:4091828-Animals,
pubmed-meshheading:4091828-Arginine Vasopressin,
pubmed-meshheading:4091828-Calcium,
pubmed-meshheading:4091828-Glucose,
pubmed-meshheading:4091828-Liver,
pubmed-meshheading:4091828-Male,
pubmed-meshheading:4091828-Oxygen Consumption,
pubmed-meshheading:4091828-Perfusion,
pubmed-meshheading:4091828-Phenylephrine,
pubmed-meshheading:4091828-Rats,
pubmed-meshheading:4091828-Rats, Inbred Strains,
pubmed-meshheading:4091828-Time Factors
|
pubmed:year |
1985
|
pubmed:articleTitle |
The Ca2+-mobilizing actions of vasopressin and angiotensin differ from those of the alpha-adrenergic agonist phenylephrine in the perfused rat liver.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|