Intracisternal galanin/angiotensin II interactions in central cardiovascular control

The aim of this work was to investigate the interactions between angiotensin II (Ang II) and galanin(1-29) [GAL(1-29)] or its N-terminal fragment galanin(1-15) [GAL(1-15)] on central cardiovascular control. The involvement of angiotensin type1 (AT1) receptor subtype was analyzed by the AT1 antagonist, DuP 753. Anesthesized male Sprague-Dawley rats received intracisternal microinjections of Ang II (3 nmol) with GAL(1-29) (3 nmol) or GAL(1-15) (0.1 nmol) alone or in combination. The changes in mean arterial pressure (MAP) and heart rate (HR) recorded from the femoral artery were analyzed. The injection of Ang II and GAL(1-15) alone did not produce any change in MAP. However, coinjections of both Ang II and GAL(1-15) elicited a significant vasopressor response. This response was blocked by DuP 753. Ang II and GAL(1-15) alone produced an increase in HR. The coinjections of Ang II with GAL(1-15) induced an increase in HR not significantly different from the tachycardia produced by each peptide. The presence of DuP 753 counteracted this response. GAL(1-29) alone elicited a transient vasopressor response that disappeared in the presence of Ang II. The coinjections of Ang II with GAL(1-29) and with DuP 753 restored the transient vasopressor effect produced by GAL(1-29). GAL(1-29) produced a slight but significant tachycardic effect that was not modified in the presence of Ang II. The presence of DuP 753 did not modify the tachycardic response produced by Ang II and GAL(1-29). These results give indications for the existence of a differential modulatory effect of Ang II with GAL(1-15) and GAL(1-29) on central blood pressure response that might be dependent on the activity of the angiotensin AT1 receptor subtype.