4.7 Article

Aortic Body Chemoreceptors Regulate Coronary Blood Flow in Conscious Control and Hypertensive Sheep

期刊

HYPERTENSION
卷 79, 期 6, 页码 1275-1285

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.121.18767

关键词

aortic bodies; arterial pressure; blood pressure; carotid body; hyperventilation; reflex

资金

  1. Health Research Council of New Zealand
  2. University of Auckland Faculty Research Development Fund
  3. National Heart Foundation of New Zealand
  4. Maurice Phyllis Paykel Trust

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This study found that activation of the aortic bodies can increase coronary blood flow, mediated by a cholinergic mechanism. In hypertensive animals, activation of the aortic bodies also increased coronary blood flow without significant difference compared to the normotensive group. However, the coronary vasodilation in hypertensive animals was affected by propranolol. These results reveal the important role of the aortic bodies in modulating coronary blood flow and the alteration of their effector mechanism in hypertension.
Background: Peripheral arterial chemoreceptors monitor the chemical composition of arterial blood and include both the carotid and aortic bodies (ABs). While the role of the carotid bodies has been extensively studied, the physiological role of the ABs remains relatively under-studied, and its role in hypertension is unexplored. We hypothesized that activation of the ABs would increase coronary blood flow in the normotensive state and that this would be mediated by the parasympathetic nerves to the heart. In addition, we determined whether the coronary blood flow response to stimulation of the ABs was altered in an ovine model of renovascular hypertension. Methods: Experiments were conducted in conscious and anesthetized ewes instrumented to record arterial pressure, coronary blood flow, and cardiac output. Two groups of animals were studied, one made hypertensive using a 2 kidney one clip model (n=6) and a sham-clipped normotensive group (n=6). Results: Activation of the ABs in the normotensive animals resulted in a significant increase in coronary blood flow, mediated, in part by a cholinergic mechanism since it was attenuated by atropine infusion. Activation of the ABs in the hypertensive animals also increased coronary blood flow (P<0.05), which was not different from the normotensive group. Interestingly, the coronary vasodilation in the hypertensive animals was not altered by blockade of muscarinic receptors but was attenuated after propranolol infusion. Conclusions: Taken together, these data suggest that the ABs play an important role in modulating coronary blood flow and that their effector mechanism is altered in hypertension.

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