Effect of Hypertension on the Response of Plasma Beta-Endorphin to the Cold Pressor Test

Abstract

Earlier reports showed that altered pain sensitivity was found in experimental hypertensive rats and hypertensive humans (Zamir and Segal 1979; Zamir and Shuber 1980), and that naloxone attenuated the analgesia of spontaneously hypertensive rats (Wendel and Bennett 1981). A number of reports showed that the hypotensive action of central alpha₂-agonists was reversed by naloxone (Petty and De Jong 1982; Farsang et al. 1980; Kunos et al. 1984) or by antiserum to beta-endorphin (Petty and De Jong 1982; Ramirez-Gonzalez et al. 1983) and that beta-endorphin caused hypotension in rats with central (Petty et al. 1981) or systemic administration (Lemaire et al. 1978). Additionally, central alpha₂-agonists were reported to increase the release of a substance with beta-endorphin like immunoreactivity from slices of brain stem of spontaneously hypertensive rats (Kunos and Farsang 1981; Naranjo et al. 1982). These observations point to a depressor role of beta-endorphin. In 1985 Casale et al. reported that the cold pressor test provoked a marked increase of plasma beta-endorphin and that the responses were the same in both young and elderly subjects, but they did not examine the effect of hypertension on the response. In order to investigate whether essential hypertensive patients may have some difference in central depressor systems, especially the beta-endorphin system, from normotensive controls, we examined the effect of the cold pressor test on plasma beta-endorphin in volunteers including patients with essential hypertension.