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R Corder

Publications and source records attributed to R Corder.

93 records · Page 6Linked to original sources

An immunoradiometric assay for the measurement of neuropeptide Y in plasma.

The development of an immunoradiometric assay (IRMA) for the direct measurement of neuropeptide Y (NPY) concentrations in plasma is reported. The assay employs simultaneous addition of 125I-labelled affinity purified sheep anti-(NPY 31-36) immunoglobulin (IgG) and a rabbit anti-NPY serum to 0.25 ml volumes of standard or unknown. After 16 hr incubation at 4 degrees C NPY-bound labelled IgG is precipitated using sheep anti-(rabbit IgG Fc region) IgG coupled to Dynospheres solid phase. Precipitated counts are proportional to the NPY concentration in samples. Using this methodology it is possible to measure basal levels in normal human subjects (range 1-5 fmol/ml). Technical difficulties encountered in raising "site-specific" antisera to NPY during the establishment of this assay are outlined.

Adrenal Gland Neoplasms↗

Attenuation of corticotropin releasing factor-induced hypotension in anesthetized rats with the CRF antagonist, alpha-helical CRF9-41; comparison with effect on ACTH release.

The effect of pretreatment with the corticotropin releasing factor (CRF-41) antagonist, alpha-helical CRF(9-41), on the hypotensive response obtained on peripheral administration of CRF-41 has been assessed in anesthetized Wistar rats. A single IV bolus dose of rat CRF-41 (2 nmol, at 0 min) produced a hypotensive effect which was rapid in onset (-52 mmHg at +1 min) and sustained throughout the 60-min study period (-42, -40, -26 and -16 mmHg at +3, +10, +30 and +60 min, respectively). The antagonist [alpha CRF(9-41)] was administered in consecutive bolus doses of 12.5, 25 and 50 nmol at -15, -10 and -5 min, respectively. This had no effect on mean arterial blood pressure (MABP) or heart rate, nor did it change significantly the magnitude of the initial rapid fall in MABP when CRF-41 was administered (-45 mmHg at +1 min). However, following pretreatment with alpha CRF(9-41), MABP returned to control values within 3 min and the sustained period of hypotension was completely blocked. Administration of CRF-41 resulted in 44% and 142% increases in norepinephrine and epinephrine measured at +60 min. Pretreatment with the antagonist attenuated the rise in circulating catecholamine levels observed after CRF-41 administration. In comparison, pretreatment with the antagonist did not alter the ACTH response to CRF-41 at +1 and +3 min and only reduced ACTH levels by 28% (p less than 0.05), 43% (p less than 0.001) and 41% (p less than 0.01) at 10, 30 and 60 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Endothelin-1 synthesis reduced by red wine.

Statistical evidence of reduced coronary heart disease in areas of high wine consumption has led to the widespread belief that wine affords a protective effect. Although moderate drinking of any alcohol helps to reduce the incidence of coronary heart disease, there is no clear evidence that red wine confers an additional benefit. Here we show that red wines strongly inhibit the synthesis of endothelin-1, a vasoactive peptide that is crucial in the development of coronary atherosclerosis. Our findings indicate that components specific to red wine may help to prevent coronary heart disease.

Animals↗