Prolonged hypoxic stimulation of carotid body chemoreceptors in cats results in sustained blood pressure and vascular resistance increases, with attenuation of respiratory and heart rate responses over time.
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Sustained pressor effects during prolonged chemoreflex stimulation may inform hypoxia-related hypertension mechanisms; leaves open human translation.
Summary Circulatory and respiratory responses to thirty minutes of hypoxic stimulation (prolonged stimulation) of the carotid body chemoreceptors were investigated in anaesthetized cats. The animals were studied in three groups: (a) animals in which the superior cervical sympathetic ganglia and aortic depressor nerves were intact, (b) animals in which the superior cervical sympathetic ganglia were removed, and (c) animals in which the aortic depressor nerves were cut. Stimulation of the carotid body chemoreceptors caused an initial increase in respiratory minute volume, bradycardia, rise in systemic arterial blood pressure and calculated total peripheral vascular resistance, with little or no change in cardiac output. With continuing stimulation the blood pressure and resistance responses were maintained, but there was attenuation of respiratory and heart rate responses. Controlling ventilation had little or no effect on the pattern of the cardiovascular responses to prolonged chemoreceptor excitation. Removal of the superior cervical ganglia had little effect on the responses to prolonged chemoreceptor stimulation with spontaneous ventilation. Section of the aortic depressor nerves had little effect on the respiratory or heart rate responses to prolonged chemoreceptor stimulation. However, the increases in blood pressure and calculated total peripheral resistance were considerably greater in the initial stages of the response, either under conditions of spontaneous ventilation or controlled ventilation, but particularly when ventilation was held constant during the period of chemoreceptor excitation.
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Carmody et al. (1974) studied this question.
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