Atrial natriuretic peptide increases cyclic guanosine monophosphate immunoreactivity in the carotid body.

The mammalian carotid body is a peripheral arterial chemoreceptor organ involved in the regulation of respiration, and in the modulation of blood pressure through reflex control of peripheral vascular resistance and cardiac output. In addition to its responsiveness to blood gases, the organ is also sensitive to hyperosmotic solutions, and we have recently shown that a systemic hormonal regulator of natriuresis and diuresis, atrial natriuretic peptide, is a potent inhibitor of chemoreceptor activity evoked by hypoxia in the cat carotid body. The present study demonstrates atrial natriuretic peptide immunoreactivity in type I cells of the carotid body, and shows further that a biologically active atrial natriuretic peptide fragment, atriopeptin III, increases cyclic guanosine monophosphate immunoreactivity in type I cells in a dose-dependent manner. Moreover, double-labeling techniques demonstrate co-existence of atrial natriuretic peptide immunoreactivity with the atriopeptin III-enhanced cyclic guanosine monophosphate reaction product. These findings indicate the probable existence of atrial natriuretic peptide receptors coupled to membrane-bound guanylate cyclase on the parenchymal type I cells. Our findings support the view that cyclic guanosine monophosphate functions as a second messenger in this organ, and may serve as a functional activity marker in identifying type I cells which respond to atrial natriuretic peptide.