CENTRALLY INFUSED GALANIN-(1-15) BUT NOT GALANIN-(1-29) REDUCES THE BARORECEPTOR REFLEX SENSITIVITY IN THE RAT

It has been demonstrated previously that central administration of the N-terminal galanin fragment (1-15) elicits hypertension and tachycard ia and antagonizes the hypotensive effect of the parent molecule galan in-(1-29). In order to further clarify the role of galanin in central cardiovascular control, the possible modulation of the baroreceptor re flex by both galanin molecules has been studied. Different groups of r ats were injected in the lateral ventricle with subthreshold doses of galanin-(1-15) (0.1 nmol/rat, or 0.3 nmol/rat), with subthreshold dose s of galanin-(1-29) (0.1 nmol/rat, and 0.3 nmol/rat) or with an effect ive dose of galanin-(1-29) (3.0 nmol/rat). The baroreceptor reflex was elicited by intravenous injections of different doses of L-phenylephr ine before and after the intraventricular administration of galanin pe ptides. The changes of the bradycardic responses after galanin peptide injections as well as the modifications of the baroreceptor reflex se nsitivity were evaluated. Intraventricular injections of galanin-(1-15 ) significantly inhibited the reflex bradycardia elicited by intraveno us L-phenylephrine and thus decreased the baroreceptor sensitivity. Ho wever, neither subthreshold doses of galanin-(1-29) nor its effective dose were able to modulate these cardiovascular responses. From these data it may be suggested that the galanin fragment(1-15) plays a more important role in central cardiovascular regulation than galanin-(1-29 ), possibly acting on a specific receptor subtype which exclusively re cognizes N-terminal fragments of galanin, and exists on cardiovascular areas of the central nervous system.