Pressor effects of endogenous opioid system during acute episodes of blood pressure increases in hypertensive patients

To investigate the involvement of endogenous opioids in acute increases in blood pressure and their functional relationship with atrial natriuretic factor and endothelin-1, we assessed plasma levels of beta-endorphin, met-enkephalin, dynorphin B, catecholamines, atrial natriuretic factor, and endothelin-1 before and after administration of the opioid antagonist naloxone hydrochloride (8 mg IV) in 28 hypertensive patients with a stress-induced acute increase in blood pressure. Ten patients with established mild or moderate essential hypertension and 10 normotensive subjects served as control groups. Opioids, atrial natriuretic factor, and endothelin-1 were radioimmunoassayed after chromatographic preextraction; catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Patients with an acute increase in blood pressure (systolic, 203.2+/-2.2 mm Hg; diastolic, 108.4+/-1.3) had plasma opioid, catecholamine, and atrial natriuretic factor levels significantly (P<.01) higher than hypertensive control patients (systolic pressure, 176.4+/-1.0 mm Hg; diastolic, 100.0+/-1.4), who had a hormonal pattern similar to that of normotensive subjects (systolic pressure, 123.2+/-1.5 mm Hg; diastolic, 75.0+/-2.0). Endothelin-1 did not differ in any group. In patients with an acute increase in blood pressure, naloxone significantly (P<.01) reduced blood pressure, heart rate, opioids, catecholamines, and atrial natriuretic factor 10 minutes after administration. Naloxone effects on blood pressure, heart rate, opioids, and catecholamines wore off within 20 minutes. In control groups, naloxone failed to modify any of the considered parameters. Our findings suggest that presser effects of opioid peptides mediated by the autonomic nervous system during stress-induced acute episodes of blood pressure increase in hypertensive patients.