Cardiopulmonary receptors and "neurogenic hypertension".

The intention of the present studies was to analyze the effects of arterial baroreceptors and cardiopulmonary receptors on cardiovascular control (I,IV,VI) and renin release (I,II,IV,V). The investigations of the role of the renin-angiotensin system on arterial pressure (III,VII) were applied to interpret a possible contribution to "neurogenic hypertension". Following conclusions are made by our findings: The partial or complete denervation of one receptor area leads to no changes in long-term arterial pressure, heart rate, plasma volume, or plasma renin activity. After sino-aortic denervation only a higher blood pressure variability is observed. Total denervation of both receptor sites increases blood pressure and its lability as well as the heart rate, although the heart rate variability remains the same. The information from arterial baroreceptors and cardiopulmonary receptors is redundant: both have an attenuating effect on the cardiovascular system but the input is not additive. "Neurogenic hypertension" is due to the denervation of both arterial baroreceptors and cardiopulmonary receptors. Arterial baroreceptor denervation alone will only increase blood pressure fluctuations. The pathway of this form of hypertension is alpha-adrenergic, the tachycardia is mediated via beta-receptors. A major role of the renin-angiotensin system or plasma volume regulation is not evident. Plasma renin activity is significantly increased, but converting-enzyme inhibition shows no obvious effect on "neurogenic hypertension". A tissue angiotensin II facilitation of the beta-adrenergic elevation of heart rate seen after total denervation is not apparent. No changes of heart rate were observed after converting-enzyme inhibition.