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Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats.
- Source :
-
American journal of physiology. Heart and circulatory physiology [Am J Physiol Heart Circ Physiol] 2012 Mar 01; Vol. 302 (5), pp. H1123-30. Date of Electronic Publication: 2011 Dec 30. - Publication Year :
- 2012
-
Abstract
- 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.
- Subjects :
- Animals
Atenolol pharmacology
Blood Pressure drug effects
Electric Stimulation
Enzyme Inhibitors pharmacology
Ganglionic Stimulants pharmacology
Indazoles pharmacology
Laser-Doppler Flowmetry
Male
Nicotine pharmacokinetics
Norepinephrine pharmacology
Propanolamines pharmacology
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Regional Blood Flow drug effects
Regional Blood Flow physiology
Superior Cervical Ganglion drug effects
Superior Cervical Ganglion physiology
Sympathetic Nervous System physiology
Tetrodotoxin pharmacology
Basilar Artery drug effects
Pons blood supply
Pons drug effects
Sympathetic Nervous System drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1522-1539
- Volume :
- 302
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- American journal of physiology. Heart and circulatory physiology
- Publication Type :
- Academic Journal
- Accession number :
- 22210747
- Full Text :
- https://doi.org/10.1152/ajpheart.01016.2011