Naturally occurring hypertension in New World nonhuman primates: Potential role of the perifornical hypothalamus.

Bibliographic Collection: 
MOCA Reference, APE
Publication Type: Journal Article
Authors: Smith, Orville A; Astley, Cliff A
Year of Publication: 2007
Journal: Am J Physiol Regul Integr Comp Physiol
Volume: 292
Issue: 2
Pagination: R937-45
Date Published: 2007 Feb
Publication Language: eng
ISSN: 0363-6119
Keywords: Animals, Aotidae, Blood Pressure, Electric Stimulation, Emotions, Female, Heart Rate, Hypertension, Hypothalamic Area, Lateral, Hypothalamus, Male, Neurons, Telemetry, Transducers
Abstract:

Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. A major impediment to the investigation into the causes of the disease is the paucity of naturally occurring animal models of the disease. There is evidence that some species of New World primates spontaneously become hypertensive. We used chronically implanted pressure transducers to assess normally occurring blood pressure and heart rate levels at rest and during routine laboratory procedures in a group of one of these New World primates (Aotus sp.). Resting mean arterial pressure ranged from 72 to 130 mmHg. Three animals were judged to have resting mean arterial pressure levels in the hypertensive range (> or =110 mmHg). In all of the animals, pressor responses to routine laboratory events were exaggerated (average highest mean pressure during 1 min from any session was 97-196 mmHg). Subsequently, the region of the perifornical/lateral hypothalamus known to produce elevated blood pressure and heart rate responses to electrical stimulation was removed, and the blood pressure responses to the laboratory routines were significantly decreased and, in some cases, eliminated. Control lesions in nearby tissue had no effect on these responses. This region may play a critical role in initiating or exacerbating cardiovascular responses that contribute to the development of essential hypertension.

DOI: 10.1152/ajpregu.00400.2006
Alternate Journal: Am. J. Physiol. Regul. Integr. Comp. Physiol.
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