Linked Life Data

943425

Source:http://linkedlifedata.com/resource/pubmed/id/943425

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1976-6-2
pubmed:abstractText
Infusion of NE in seven normal subjects and 13 patients with essential or renal hypertension caused a pronounced initial rise of systolic pressure in only seven hypertensives and one normotensive. This hyperresponsiveness was not a constant finding in essential or renal hypertensives but usually occurred in patients with highest preinfusion pressures. In some of the latter, following the pronounced rise in pressure when NE infusion was started (0.05 mug/kg/min), pressure did not increase further (probably due to reflexly reduced cardiac output) despite progressively increasing the infusion rate to 0.1 and 0.2 mug/kg/min. Hyperresponsiveness could not be attributed to increased NE concentrations at receptor sites since it was not significantly correlated with elevations of NE plasma concentrations; in some essential hypertensives, mild pressure increases occurred despite marked elevations of arterial plasma NE. Since hyperresponsiveness occurred in some patients with essential and some with renal hypertension, it could not be used to differentiate these two groups of hypertensives. The mechanism for hyperresponsiveness remains unclear but may be better explained by vascular structure alterations than by hyperreactive vascular smooth muscle per se; however, a combination of these factors could participate. During NE infusion, reflex bradycardia was associated with elevated pressure and was slightly more pronounced in normotensives; this was probably related to diminished baroreflex sensitivity in essential hypertensives and due to "resetting" of their baroreceptors. During high rates of NE infusion (0.2 mu/kg/min), higher arterial plasma NE concentrations in essential hypertensives than in normotensives could result from reduction in blood flow to organs important in inactivating circulating NE; however, a defective inactivating mechanism for NE in some essential hypertensives cannot be totally excluded.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0091-2700
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-41
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Norepinephrine infusion in normal subjects and patients with essential or renal hypertension: effect on blood pressure, heart rate, and plasma catecholamine concentrations.
pubmed:publicationType
Journal Article