Contribution of baroreceptor reflexes to blood pressure and sympathetic responses to cholecystokinin and vasoactive intestinal peptide in anesthetized dogs

• Published in: European journal of pharmacology Vol. 175; no. 3; p. 245
• Main Authors: Koyama, S, Fujita, T, Shibamoto, T, Matsuda, Y, Uematsu, H, Jones, R O
• Format: Journal Article
• Language: English
• Published: Netherlands 17.01.1990
• Subjects: Anesthesia; Animals; Blood Pressure - drug effects; Cholecystokinin - pharmacology; Dogs; Injections, Intravenous; Kidney - innervation; Nitroprusside - pharmacology; Phenylephrine - pharmacology; Pressoreceptors - drug effects; Reflex - drug effects; Sympathetic Nervous System - drug effects; Vagotomy; Vasoactive Intestinal Peptide - administration & dosage; Vasoactive Intestinal Peptide - pharmacology
• ISSN: 0014-2999
• DOI: 10.1016/0014-2999(90)90561-J

The effects of synthetic vasoactive intestinal peptide (VIP) and cholecystokinin (CCK) on systemic blood pressure and renal nerve activity were studied before and after cervical vagotomy, and sino-aortic denervation with vagotomy in anesthetized dogs. Intravenous injection of VIP (5 micrograms/kg) in animals with an intact neuraxis produced a significant decrease in systemic blood pressure and a significant increase in renal nerve activity. These responses to VIP did not change after vagotomy and after complete denervation, VIP did not cause any change in renal nerve activity, even during hypotension. The level of hypotension after complete denervation was greater than that under other conditions. These results indicate that the cardiovascular effects of VIP are reduced by activation of the systemic baroreceptors. Intravenous injection of CCK (10 micrograms/kg) in animals with an intact neuraxis produced significant decreases in blood pressure and renal nerve activity. These responses to CCK were abolished in animals with cervical vagotomy only. However, following complete denervation of the carotid sinus and total section of the vagal nerves, CCK caused a significant increase in blood pressure and renal sympathetic nerve activity. These results indicate that the sympathetic depressor effect of CCK may be mediated by activation of the vagal afferents, and that the sympathetic pressor effect may be due to a direct action of CCK on the central nervous system. Thus, each gastrointestinal peptide may regulate the cardiovascular system through a different mechanism.