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|Title:||Intrarenal Adrenergic Mechanisms Controlling Renin Release|
|Author(s):||Opgenorth, Terry John|
|Department / Program:||Physiology and Biophysics|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Subject(s):||Biology, Animal Physiology|
|Abstract:||These studies were undertaken to investigate the role of alpha- and beta-adrenoceptors in the control of renin release. In addition, the function of calcium in the adrenergic control of renin release was examined. All studies were carried out in the isolated, nonfiltering, constant-pressure perfused rabbit kidney.
Isoproterenol, a beta-agonist, infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g kw increased (p < 0.05) renin secretion from the kidney in a dose-dependent manner. Propranolol (5.0 nM/min/g kw), a beta-agonist, blocked this response. Phenylephrine, an alpha-agonist, infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g kw did not alter renin release from the isolated perfused rabbit kidney. However, phenylephrine (5.0 nM/min/g kw) did block the renin response to isoproterenol infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g kw. Thus, it was concluded that alpha-adrenoceptor activation blocks the renin response to beta-adrenoceptor activiation.
The renin response to isoproterenol was accentuated when calcium was removed and chelated from the perfusate. In contrast, the inhibitory effect of phenylephrine on isoproterenol-evoked renin release was masked when calcium was absent from the perfusate. In addition, D-600 (5 x 10('-7)), a blocker of voltage-dependent calcium channels, masked the inhibition of isoproterenol-evoked renin release by phenylephrine when calcium was present in the perfusate. Therefore, it was concluded that the alpha-adrenoceptor inhibition of beta-adrenoceptor stimulated renin release is dependent on the influx of calcium into the JG cells through voltage-dependent calcium channels.
Based on the observations made in these experiments and on the current literature, it is hypothesized that consequent to beta-adrenergic activation, prostaglandins mediate an increase in adenylate cyclase activity. The result being an increase in intracellular cAMP which would stimulate Na-K ATPase activity. Intracellular sodium would decrease, stimulating Na-K exchange, thereby lowering intracellular free calcium and stimulating renin release. On the other hand, alpha-adrenoceptor activation would open calcium channels, thereby allowing calcium to move down its electrochemical gradient into the JG cell and inhibit renin release. How intracellular calcium affects renin release is not known.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1982.
|Date Available in IDEALS:||2014-12-16|
This item appears in the following Collection(s)
Dissertations and Theses - Molecular and Integrative Physiology
Graduate Dissertations and Theses at Illinois
Graduate Theses and Dissertations at Illinois