Plasma concentration and vascular effect of β-endorphin in spontaneously hypertensive and Wistar Kyoto rats

Summary

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