Coronary vasoconstriction during stimulation in hypothalamic defense region. Am J Physiol 1991 Feb;260(2 Pt 2):R335-45
Date
02/01/1991Pubmed ID
1996721DOI
10.1152/ajpregu.1991.260.2.R335Scopus ID
2-s2.0-0025967706 (requires institutional sign-in at Scopus site) 16 CitationsAbstract
Previous studies have identified a site in lateral hypothalamus (LH) in which electrical stimulation elicits coronary vasoconstriction. We injected the retrogradely transported tracer Fast Blue to determine which brain regions project to LH. Projections to or through LH were found from the paraventricular nucleus (PVN) of the hypothalamus, bed nucleus of the stria terminalis (BNST), and dorsal raphe nucleus (DRN). In chloralose-anesthetized cats, electrical stimulation in DRN and BNST failed to increase coronary vascular resistance (CVR). However, stimulation lateral to PVN in the anterior hypothalamic area (AHA), a region not labeled by the tracer, caused a transient decrease in coronary blood flow similar to that elicited from LH. The increase in CVR was accompanied by hemodynamic changes that are characteristic of the defense reaction including a cholinergically mediated decrease in hindquarter vascular resistance. This response is likely due to activation of fibers of passage and not cell bodies, since cell bodies in the region were not retrogradely labeled and coronary vasoconstriction was not seen following microinjection of several excitatory amino acids into AHA. These data suggest that coronary vasoconstriction may be a component of the defense reaction elicited by electrical activation of AHA.
Author List
Arthur JM, Bonham AC, Gutterman DD, Gebhart GF, Marcus ML, Brody MJAuthor
David Gutterman MD Emeritus Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AmidinesAnimals
Atropine
Cats
Coronary Vessels
Defense Mechanisms
Electric Stimulation
Fluorescent Dyes
Ganglia, Sympathetic
Ganglionectomy
Hypothalamus
Male
Prazosin
Vasoconstriction
