Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.

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Mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded in conscious spontaneously hypertensive rats (SHR). Infusion of metoprolol (4 μmol kg−1 h−1) or propranolol (1.5 μmol kg−1 h−1) reduced HR and significantly increased RSNA. Administration of metoprolol caused a sustained decrease of MAP starting in the third hour of infusion. In contrast, administration of propranolol induced a biphasic response in MAP. It is suggested that the increase of RSNA after both β‐adrenoceptor blocking drugs is due to a decrease in arterial baroreceptor activity.

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