Plasma concentration and vascular effect of beta-endorphin in spontaneously XXXX and @entity35 Kyoto @entity35 .

@entity35 @entity9210 @entity101 @entity3317
In order to find out whether beta-endorphin (beta-E) is involved in the development of @entity101 , we performed two series of experiments. Firstly, spontaneously @entity101 @entity35 (SHR) and their normotensive @entity35 Kyoto controls (WKY) were submitted to ether stress. Plasma concentrations of beta-endorphin-like immunoreactivity (beta-EI), @entity3317 (ACTH) and @entity9210 ) were measured by radioimmunoassay. The basal concentration of beta-EI was similar in WKY and SHR, whereas WKY had higher levels of ACTH and lower levels of @entity9210 than SHR. In both strains acute stress enhanced the plasma concentration of beta-EI to the same extent and with a similar time-course. The increase of plasma beta-EI coincided with a rise in ACTH but not @entity9210 . Gel chromatography of beta-EI revealed that plasma extracts contain similar amounts of beta-lipotropin- (beta-LPH) and beta-E-sized immunoreactive components, and that acute stress elevated both forms of beta-EI. Secondly, isolated tail arteries of SHR and WKY were perfused and field stimulated with two pulses at 1 Hz. beta-E depressed stimulation-evoked vasoconstriction with the same potency in both strains. Thus, basal and stress-induced levels of beta-EI did not differ in SHR and WKY. Moreover, in the tail artery of both strains the sensitivity of presynaptic opioid receptors towards beta-E was almost identical. If the beta-E sensitivity of these receptors in other arteries of WKY and SHR is also similar a major role of the circulating peptide in the development of @entity101 is rather unlikely.
