Sympathetic nerve‐mediated nitrergic dilation of basilar arteries of the rat in vivo

• Published in: The FASEB journal 2010-04, Vol.24 (S1), p.lb527-lb527
• Main Authors: Chang, Hsi‐Hsien, Lee, Hui‐Chao, Chen, Po‐Yi, Lee, Yuan‐Chieh, Chen, Mei‐Fang, Kuo, Jon‐Son, Lee, Tony Jer‐Fu
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.24.1_supplement.lb527

Brain arteries receive sympathetic nerves originating in superior cervical ganglion (SCG), and norepinephrine (NE) is thought the transmitter for vasoconstriction. The exact role of the sympathetic nerve in regulating brain circulation, however, remains unclear. Results of studies in isolated cerebral arteries indicate that activation by nicotine of cerebral perivascular sympathetic nerves induces NE release. NE then diffuses to act on β2‐adrenoceptors located on nitrergic nerve terminals to release nitric oxide (NO) that relaxes the smooth muscle. This axo‐axonal interaction in regulating cerebral blood flow, therefore, was examined in the rat in vivo. Electrical stimulation of SCG caused dilation of basilar arteries in anesthetized normotensive Wistar‐Kyoto rats (WKY). The vasodilation was blocked by inhibitors for NO synthesis and beta2‐adrenoceptors. In spontaneously hypertensive rats (SHRs), electrical stimulation‐of‐SCG‐induced nitrergic dilation of basilar arteries, however, was diminished. This is consistent with reported findings of decreased parasympathetic nerve terminals in cerebral arteries of SHR. These findings indicate that activation of cerebral perivascular sympathetic nerves does not cause significant vasoconstriction, but predominant nitrergic dilation of the basilar arteries in normotensive animals. This effect of sympathetic nerves may change in hypertension.