摘要
The aim of this work was to investigate the interactions between angiotensin II (Ang II) and galanin(1芒芒芒29) [GAL(1芒芒芒29)] or its N-terminal fragment galanin(1芒芒芒15) [GAL(1芒芒芒15)] on central cardiovascular control. The involvement of angiotensin type1 (AT1) receptor subtype was analyzed by the AT1 antagonist, DuP 753. Anesthesized male Sprague芒芒芒Dawley rats received intracisternal microinjections of Ang II (3 nmol) with GAL(1芒芒芒29) (3 nmol) or GAL(1芒芒芒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芒芒芒15) alone did not produce any change in MAP. However, coinjections of both Ang II and GAL(1芒芒芒15) elicited a significant vasopressor response. This response was blocked by DuP 753. Ang II and GAL(1芒芒芒15) alone produced an increase in HR. The coinjections of Ang II with GAL(1芒芒芒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芒芒芒29) alone elicited a transient vasopressor response that disappeared in the presence of Ang II. The coinjections of Ang II with GAL(1芒芒芒29) and with DuP 753 restored the transient vasopressor effect produced by GAL(1芒芒芒29). GAL(1芒芒芒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芒芒芒29). These results give indications for the existence of a differential modulatory effect of Ang II with GAL(1芒芒芒15) and GAL(1-29) on central blood pressure response that might be dependent on the activity of the angiotensin AT1 receptor subtype.