Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats.
The close apposition between sympathetic and parasympathetic nerve terminals in the adventitia of cerebral arteries provides morphological evidence that sympathetic nerve activation causes parasympathetic nitrergic vasodilation via a sympathetic-parasympathetic interaction mechanism. The decreased parasympathetic nerve terminals in basilar arteries (BA) of spontaneously hypertensive rat (SHR) and renovascular hypertensive rats (RHR) compared with Wistar-Kyoto rats (WKY), therefore, would diminish this axo-axonal interaction-mediated neurogenic vasodilation in hypertension. Increased basilar arterial blood flow (BABF) via axo-axonal interaction during sympathetic activation was, therefore, examined in anesthetized rats by laser-Doppler flowmetry. Electrical stimulation (ES) of sympathetic nerves originating in superior cervical ganglion (SCG) and topical nicotine (10-30 μM) onto BA of WKY significantly increased BABF. Both increases were inhibited by tetrodotoxin, 7-nitroindazole (neuronal nitric oxide synthase inhibitor), and ICI-118,551 (β(2)-adrenoceptor antagonist), but not by atenolol (β(1)-adrenoceptor antagonist). Topical norepinephrine onto BA also increased BABF, which was abolished by atenolol combined with 7-nitroindazole or ICI-118,551. Similar results were found in prehypertensive SHR. However, in adult SHR and RHR, ES of sympathetic nerves or topical nicotine caused minimum or no increase of BABF. It is concluded that excitation of sympathetic nerves to BA in WKY causes parasympathetic nitrergic vasodilation with increased BABF. This finding indicates an endowed functional neurogenic mechanism for increasing the BABF or brain stem blood flow in coping with increased local sympathetic activities in acutely stressful situations such as the "fight-or-flight response." This increased blood flow in defensive mechanism diminishes in genetic and nongenetic hypertensive rats due most likely to decreased parasympathetic nitrergic nerve terminals.
Institute of Medical Sciences, College of Medicine, Tzu Chi University, Hualien, Taiwan.
Hsi-Hsien
HH
Chang
Yuan-Chieh
YC
Lee
Mei-Fang
MF
Chen
Jon-Son
JS
Kuo
Tony J F
TJ
Lee
D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001488:Basilar Artery / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005731:Ganglionic Stimulants / Q000494:pharmacology; D007191:Indazoles / Q000494:pharmacology; D017078:Laser-Doppler Flowmetry; D008297:Male; D009538:Nicotine / Q000493:pharmacokinetics; D009638:Norepinephrine / Q000494:pharmacology; D011149:Pons / Q000098:blood supply* / Q000187:drug effects*; D011412:Propanolamines / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D017783:Superior Cervical Ganglion / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D004791:Enzyme Inhibitors; D005731:Ganglionic Stimulants; D007191:Indazoles; D011412:Propanolamines; D013779:Tetrodotoxin; C026777:ICI 118551; D001262:Atenolol; D009538:Nicotine; C080122:7-nitroindazole; D009638:Norepinephrine