4.5 Article

Acute reductions in blood flow restricted to the dorsomedial medulla induce a pressor response in rats

期刊

JOURNAL OF HYPERTENSION
卷 29, 期 8, 页码 1536-1545

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0b013e3283484106

关键词

heme oxygenase-1; hypertension; hypoxia; nucleus tractus solitarii

资金

  1. Japan Society for the Promotion of Science [21300253, 19599022, 19-07458]
  2. Takeda Science Foundation
  3. British Heart Foundation
  4. Royal Society
  5. Grants-in-Aid for Scientific Research [19599022, 21300253] Funding Source: KAKEN
  6. British Heart Foundation [RG/07/006/23634] Funding Source: researchfish

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Objectives The brainstem nucleus of the solitary tract (nucleus tractus solitarii, NTS) is a pivotal region for regulating the set-point of arterial pressure, the mechanisms of which are not fully understood. Based on evidence that the NTS exhibits O-2-sensing mechanisms, we examined whether a localized disturbance of blood supply, resulting in hypoxia in the NTS, would lead to an acute increase in arterial pressure. Methods Male Wistar rats were used. Cardiovascular parameters were measured before and after specific branches of superficial dorsal medullary veins were occluded; we assumed these were drainage vessels from the NTS and would produce stagnant hypoxia. Hypoxyprobe-1, a marker for detecting cellular hypoxia in the post-mortem tissue, was used to reveal whether vessel occlusion induced hypoxia within the NTS. Results Following vessel occlusion, blood flow in the dorsal surface of the medulla oblongata including the NTS region showed an approximately 60% decrease and was associated with hypoxia in neurons located predominantly in the caudal part of the NTS as revealed using hypoxyprobe-1. Arterial pressure increased and this response was pronounced significantly in both magnitude and duration when baroreceptor reflex afferents were sectioned. Conclusion These results suggest that localized hypoxia in the NTS increases arterial pressure. We suggest this represents a protective mechanism whereby the elevated systemic pressure is a compensatory mechanism to enhance cerebral perfusion. Whether this physiological mechanism has any relevance to neurogenic hypertension is discussed. J Hypertens 29: 1536-1545 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

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