Role of Calcium and Beta-Adrenergic System in Control of Parathyroid Hormone Secretion

1976 ◽  
Vol 151 (2) ◽  
pp. 326-328 ◽  
Author(s):  
S. C. Kukreja ◽  
P. A. Johnson ◽  
G. Ayala ◽  
P. Banerjee ◽  
E. N. Bowser ◽  
...  
1977 ◽  
Vol 43 (4) ◽  
pp. 612-616 ◽  
Author(s):  
R. J. Porcelli ◽  
A. T. Viau ◽  
N. E. Naftchi ◽  
E. H. Bergofsky

The role of the adrenergic receptor in mediating pulmonary vascular responses to gaseous and humoral agents was investigated by use of epinephrine injections in the perfused feline pulmonary circulation. Alteration of the balance between alpha- and beta-adrenergic activity was quantified by measurement of decreasing vasoconstrictor activity to epinephrine and rising lobar tissue 3′,5′-adenosine cyclic monophosphate (cAMP) levels. The increased beta-adrenergic activity thus generated was associated with marked reductions in the pulmonary vasoconstrictor responses to hypoxia, hypercapnic acidosis, and histamine, but not to serotonin. Repeated pulmonary vasodilations or increases in blood, but not pulmonary tissue, levels of cAMP induced by theophylline doses, which would not necessarily affect the beta-adrenergic activity, did not alter the pulmonary vasoconstrictor responses to hypoxia, hypercapnia, or histamine. These data support the significant role which the adrenergic system plays in mediating pulmonary vasoconstrictor responses to certain specific gaseous and humoral agents, and the specificity with which this mediation occurs serves to link hypoxia and histamine together so that the latter could serve as a mediator of the former.


Bone ◽  
1995 ◽  
Vol 16 (4) ◽  
pp. S365-S372 ◽  
Author(s):  
S.L. Pocotte ◽  
G. Ehrenstein ◽  
L.A. Fitzpatrick

1990 ◽  
Vol 258 (1) ◽  
pp. R120-R123
Author(s):  
A. Rybczynska ◽  
A. Hoppe ◽  
F. G. Knox

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone (PTH). The present study evaluated the role of the beta-adrenergic system in this resistance phenomenon. In clearance experiments performed on acutely thyroparathyroidectomized male Sprague-Dawley rats, the phosphaturic response to PTH was determined in the presence and absence of propranolol in rats fed a low-phosphate diet (LPD) for 0.5, 1, 2, 3, or 4 days. Fractional excretion of phosphate (FEPi) in control rats fed a normal-phosphate diet (NPD) increased from 4.37 +/- 1.6 to 38.5 +/- 3.4% in response to PTH infusion. Propranolol did not change FEPi in NPD animals in the absence or in the presence of PTH (2.0 +/- 1.1 vs. 36.7 +/- 1.6%). LPD resulted in a gradual decrease in the phosphaturic response to PTH infusion as compared with NPD animals. PTH increased FEPi to 24.2 +/- 6.0% after one-half day of LPD, but when the infusion was supplemented with propranolol, PTH increased FEPi to 38.0 +/- 4.7%, similar to that in NPD animals. In the group fed LPD for one day, PTH increased FEPi to 16.9 +/- 4.3%, whereas in the presence of propranolol FEPi was restored to a similar level as in the NPD group (36.0 +/- 5.9%). Two days of LPD markedly decreased FEPi in response to PTH to 7.9 +/- 3.8% as compared with NPD rats, and propranolol infusion did not change this value significantly. Three and 4 days of LPD induced complete resistance to the phosphaturic effect of PTH in the presence as well as in the absence of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)


Endocrinology ◽  
1982 ◽  
Vol 111 (1) ◽  
pp. 225-230 ◽  
Author(s):  
MARCOS ROTHSTEIN ◽  
JEREMIAH MORRISSEY ◽  
EDUARDO SLATOPOLSKY ◽  
SAULO KLAHR

1975 ◽  
Vol 40 (3) ◽  
pp. 478-481 ◽  
Author(s):  
SUBHASH C. KUKREJA ◽  
GARY K. HARGIS ◽  
E. NELSON BOWSER ◽  
WALTER J. HENDERSON ◽  
ELMER W. FISHERMAN ◽  
...  

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