TY - JOUR
T1 - Mineralocorticoid-induced increase in β-adrenergic receptors of cultured rat arterial smooth muscle cells
AU - Jazayeri, Allahyar
AU - Meyer, Walter J.
N1 - Funding Information:
Acknowledgemen&--This work was supported by NIH Grant DHHS 5ROl HL 20201-0a6n d theD epartmenotf Psychiatry, The University of Texas Me&al Branch, Galveston, Texas. A.J. was supportedb y an American Heart AssociationM edical StudentF ellowshipG rant.
Funding Information:
the Clinical Research Center Program, grant No. RR73, UTMB, Galveston).
PY - 1989/11
Y1 - 1989/11
N2 - We have investigated the effect of mineralocorticoids on β-adrenergic receptors in cultured arterial smooth muscle cells. Mineralocorticoid (aldosterone) treatment resulted in a significant increase in β-adrenergic receptors measured by [3H]dihydroalprenolol (DHA) binding. This effect required at least 20 hours of incubation with aldosterone and was completely blocked by cycloheximide (10 μg/ml), indicating protein synthesis was required for this response. Aldosterone at the concentration range of 10-8-10-6M increased [3H]DHA binding, but was ineffective at 10-9 M. Scatchard analysis of [3H]DHA binding revealed that the observed significant increase in binding was due to an increased number of binding sites (P < 0.05), and that the affinity was unchanged. The aldosterone (1 × 10-8 M) effect was completely blocked by the combination of RU 38486 (10-6M) and spironolactone (10-7 M), but not by the glucocorticoid antagonist RU 38486 alone. While basal c-AMP levels were not changed by aldosterone (10-6 M) treatment, the isoproterenol (10-6 M) stimulated level of c-AMP was significantly higher in cells treated with aldosterone (P < 0.05). We conclude that aldosterone, acting through the mineralocorticoid receptor, has a direct effect on arterial smooth muscle cells mediated through modulation of β-adrenergic receptors of these cells.
AB - We have investigated the effect of mineralocorticoids on β-adrenergic receptors in cultured arterial smooth muscle cells. Mineralocorticoid (aldosterone) treatment resulted in a significant increase in β-adrenergic receptors measured by [3H]dihydroalprenolol (DHA) binding. This effect required at least 20 hours of incubation with aldosterone and was completely blocked by cycloheximide (10 μg/ml), indicating protein synthesis was required for this response. Aldosterone at the concentration range of 10-8-10-6M increased [3H]DHA binding, but was ineffective at 10-9 M. Scatchard analysis of [3H]DHA binding revealed that the observed significant increase in binding was due to an increased number of binding sites (P < 0.05), and that the affinity was unchanged. The aldosterone (1 × 10-8 M) effect was completely blocked by the combination of RU 38486 (10-6M) and spironolactone (10-7 M), but not by the glucocorticoid antagonist RU 38486 alone. While basal c-AMP levels were not changed by aldosterone (10-6 M) treatment, the isoproterenol (10-6 M) stimulated level of c-AMP was significantly higher in cells treated with aldosterone (P < 0.05). We conclude that aldosterone, acting through the mineralocorticoid receptor, has a direct effect on arterial smooth muscle cells mediated through modulation of β-adrenergic receptors of these cells.
UR - http://www.scopus.com/inward/record.url?scp=0024801861&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0024801861&partnerID=8YFLogxK
U2 - 10.1016/0022-4731(89)90250-1
DO - 10.1016/0022-4731(89)90250-1
M3 - Article
C2 - 2557490
AN - SCOPUS:0024801861
SN - 0022-4731
VL - 33
SP - 987
EP - 991
JO - Journal of Steroid Biochemistry
JF - Journal of Steroid Biochemistry
IS - 5
ER -