Angiotensin II increases afferent discharge from the carotid body in vitro.
We hypothesized that angiotensin II receptors (AT receptors) are expressed
functionally in the type-I cell of the carotid body. Cytosolic free [Ca2+]
([Ca2+](i)) in type-I cells freshly dissociated from rat carotid bodies wa
s measured spectrofluorimetrically. Angiotensin II (10-100 nM) concentratio
n-dependently increased [Ca2+](i) in type-I cells. The [Ca2+](i) response w
as blocked by pretreatment with losartan (1 muM), an AT(1) receptor antagon
ist, but not by blockade of AT(2) receptors with PD-123319 (1 muM). Moreove
r, the gene expression of AT(1) receptors was assessed by the reverse trans
criptase polymerase chain reaction and gene transcripts of both AT(1a) and
AT(1b) receptors were detected in the carotid body. In addition, immunohist
ochemical study revealed that AT(1) immunoreactivity was localized in lobul
es of type-I cells in the carotid body. Taken together, these results sugge
st that type-I cells in the rat carotid body express functional angiotensin
II receptors. The binding of angiotensin II to the AT(1) receptors increas
es [Ca2+](i), a key step of the intracellular signalling cascade following
the activation of the receptors. It is concluded that angiotensin II modula
tes carotid body chemoreceptor function directly via AT(1) receptors in the
type-I cell.