Modification of the cardiovascular response to enkephalin by preoptic-hypothalamic periventricular lesions

The cardiovascular effects of central and peripheral injection of [D-Ala2]-methionine-enkephalin were examined in rats with electrolytic lesions of anteroventral third ventricle periventricular tissue (AV3V). Sham-operated rats demonstrated a biphasic increase in blood pressure and a tachycardia after intracerebroventricular injection and an increase in blood pressure following intravenous injection. AV3V-lesions blunted the initial component of the central pressor response but did not affect the peripheral response. The AV3V region appears to mediate a portion of the blood pressure response to central enkephalin. The cardiovascular effects of enkephalin are complex and are probably mediated by more than one locus in the central nervous system. Intracerebroventricular (icv) and intravenous (iv) injections of the methionine-enkephalin analogue [D-Ala2]-met-enkephalin (DAME) increase blood pressure in conscious rats (Rockhold, Crofton and Share, 1981). However, the central nervous system sites upon which enkephalins act to cause cardiovascular changes are not yet defined. A circumventricular organ, the organum vasculosum of the lamina terminalis (OVLT), is of particular interest in this regard. The OVLT contains neuronal elements which demonstrate enkephalin-like immunoreactivity (Finley, Maderdrut and Petrusz, 1980) and electrolytic lesions of periventricular tissue of the antero-ventral third ventricle (AV3V) region (which includes the OVLT) abolish the pressor response to icv administration of another peptide hormone, angiotensin II (Bealer, Phillips, Johnson and Schmid, 1979). Such data suggest that the AV3V region may play a role in enkephalin-induced cardiovascular changes. The present investigation examines cardiovascular effects following icv and iv administration of DAME in sham-operated and AV3V-lesioned rats.