Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction. Am J Physiol 1991 Nov;261(5 Pt 2):H1585-96
Date
11/11/1991Pubmed ID
1683174DOI
10.1152/ajpheart.1991.261.5.H1585Scopus ID
2-s2.0-0026343042 (requires institutional sign-in at Scopus site) 15 CitationsAbstract
A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.
Author List
Miller FJ Jr, Marcus ML, Brody MJ, Gutterman DDMESH terms used to index this publication - Major topics in bold
AnimalsAutonomic Nervous System
Blood Flow Velocity
Blood Pressure
Cats
Coronary Circulation
Coronary Vessels
Female
Ganglia, Autonomic
Glutamates
Glutamic Acid
Heart Rate
Hindlimb
Kainic Acid
Male
Muscle, Smooth, Vascular
Muscles
Prazosin
Propranolol
Receptors, Adrenergic, alpha
Vascular Resistance
Vasoconstriction