| Subject | Predicate | Object | Context |
|---|---|---|---|
| pubmed-article:3571525 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3571525 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:3571525 | lifeskim:mentions | umls-concept:C0021640 | lld:lifeskim |
| pubmed-article:3571525 | lifeskim:mentions | umls-concept:C0007227 | lld:lifeskim |
| pubmed-article:3571525 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3571525 | pubmed:dateCreated | 1987-5-27 | lld:pubmed |
| pubmed-article:3571525 | pubmed:abstractText | We sought to determine whether the insular cortex contributes to the regulation of arterial blood pressure (AP). Responses to electrical and chemical stimulation of the cortex were studied in the anesthetized, paralyzed, and artificially ventilated Sprague-Dawley rat. The insular cortex was initially defined, anatomically, by the distributions of retrogradely labeled perikarya following injections of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the nucleus tractus solitarii (NTS). Injections of WGA-HRP into the insular cortex anterogradely labeled terminals in cardiopulmonary and other divisions of the NTS and confirmed projections revealed by retrograde tracing experiments. Electrical stimulation of the insular cortex elicited elevations of AP (less than or equal to 50 mm Hg) and cardioacceleration (less than or equal to 40 bpm). The locations of the most active pressor sites corresponded closely to the locations of retrogradely labeled cells in layer V of granular and posterior agranular areas of the insular cortex (areas 14 and 13) and the extreme capsule. Maximal pressor responses were obtained at a stimulus intensity of three to five times threshold current of 20-30 microA. Responses elicited mostly with higher-threshold currents were also mapped in areas 2a and 5lb and the claustrum and within the corpus callosum. Unilateral injections into the insular pressor area of the excitatory amino acid monosodium glutamate (L-Glu; 0.05 nmol to 10 nmol) or the rigid structural analogue of L-Glu, kainic acid (KA) (0.4 nmol) (which specifically excite perikarya), caused topographically specific elevations in AP and tachycardia. During the course of the anatomical transport studies, new findings were obtained on the organization and characteristics of the cortical innervation of the NTS and the nucleus reticularis parvocellularis. Topographic relationships between the cortex and the NTS were organized in a more complex manner than previously thought. Cells projecting to caudal cardiopulmonary segments of the NTS were fewer and generally located ventrally and caudally and in a more restricted area than cells projecting rostrally or to the parvicellular reticular formation. Anterograde transport data revealed new presumptive terminal fields in dorsolateral, ventral, periventricular, and commissural regions of the NTS, including an area overlapping the terminal field of the aortic baroreceptor nerve. We conclude that neurons within an area of the insular cortex projecting to multiple brainstem autonomic nuclei, including a region of the NTS innervated by baroreceptor afferents, increase arterial blood pressure and heart rate.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
| pubmed-article:3571525 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3571525 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3571525 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3571525 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3571525 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:3571525 | pubmed:issn | 0021-9967 | lld:pubmed |
| pubmed-article:3571525 | pubmed:author | pubmed-author:ReisD JDJ | lld:pubmed |
| pubmed-article:3571525 | pubmed:author | pubmed-author:AnwarMM | lld:pubmed |
| pubmed-article:3571525 | pubmed:author | pubmed-author:GranataA RAR | lld:pubmed |
| pubmed-article:3571525 | pubmed:author | pubmed-author:RuggieroD ADA | lld:pubmed |
| pubmed-article:3571525 | pubmed:author | pubmed-author:MraovitchSS | lld:pubmed |
| pubmed-article:3571525 | pubmed:issnType | lld:pubmed | |
| pubmed-article:3571525 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:3571525 | pubmed:volume | 257 | lld:pubmed |
| pubmed-article:3571525 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3571525 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3571525 | pubmed:pagination | 189-207 | lld:pubmed |
| pubmed-article:3571525 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:meshHeading | pubmed-meshheading:3571525-... | lld:pubmed |
| pubmed-article:3571525 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:3571525 | pubmed:articleTitle | A role of insular cortex in cardiovascular function. | lld:pubmed |
| pubmed-article:3571525 | pubmed:publicationType | Journal Article | lld:pubmed |
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