1. PTHrP enhances the secretory response of PTH to a hypocalcemic stimulus in rat parathyroid glands 
Ewa Lewin, Yolanda Almaden, Mariano Rodriguez, Klaus Olgaard 
Kidney International 
Volume 58, Issue 1, Pages (July 2000)
DOI: /j x
Copyright © 2000 International Society of Nephrology Terms and Conditions

2. Figure 1
Detection of rat parathyroid hormone (PTH) 1-84 (▪), parathyroid hormone-related peptide (PTHrP) 1-40 (▾), PTHrP 1-86 (▾), and the bovine PTH inhibitor [(Tyr34)bPTH-(7-34)amide] (□) in the rat PTH (IRMA) assay. The PTHrP fragments were not detected in the assay.
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

3. Figure 2
The Ca++/PTH relationship during an acute induction of hypocalcemia by an EGTA infusion in the rat. The transient pattern of the initial increase of PTH secretion in response to the reduction of plasma Ca++ is shown (N = 6, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

4. Figure 3
Effect of PTHrP on the secretory response of PTH to an acute induction of hypocalcemia (A) induced by an EGTA infusion. The rate of reduction of p-Ca++ was similar in all groups of rats (B). A bolus of PTHrP 1-40 (▴), PTHrP 1-86 (▾), or vehicle (▪) was injected at time 0. PTHrP significantly enhanced (P < 0.001) the low-Ca++–stimulated PTH secretion in vivo (N = 6 in each group, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

5. Figure 4
Ca++/PTH relationship during hyper-, normo-, and hypocalcemia in rats receiving PTHrP 1-40 (▪) or vehicle (□). A bolus of PTHrP or vehicle was given to the rats after hypercalcemia was induced by a Ca++ infusion. Then, Ca++ was gradually reduced by an EGTA infusion. Arrow on the absissa depicts the direction of change in p-Ca++. During hypercalcemia and normocalcemia, PTH levels were not influenced by PTHrP, while in hypocalcemia, PTHrP significantly enhanced the PTH levels (P < 0.001, N = 6 in each group, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

6. Figure 5
Effect of PTHrP on the peripheral metabolism of PTH. Synthetic human PTH 1-84 (hPTH; 3.5 ng) was injected together with 100 μg of PTHrP 1-40 (♦) or vehicle (▴) into the rat. Plasma levels of hPTH were measured by an intact hPTH IRMA assay, which does not cross react with rat PTH. The disappearance of hPTH 1-84 was not affected by PTHrP (N = 8 in each group, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

7. Figure 6
Effect of an acute 50% reduction of the parathyroid mass on the plasma PTH levels (A) during EGTA-induced hypocalcemia. Unilateral parathyroidectomy (UPTX) was performed just before (▪) or after 30 minutes of EGTA infusion (□). Control rats were not UPTX (▿). The arrows depict the time of UPTX, which reduced the glandular mass and the plasma PTH levels by 50%. A similar rate of reduction of p-Ca++ was obtained in all groups of rats (B). (N = 6 in each group, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions

8. Figure 7
Effect of PTHrP 1-40 on normal- and low-Ca++–stimulated PTH secretion in vitro from whole rat parathyroid glands. PTH secretion was significantly stimulated (P < 0.002) by a low Ca++ concentration of 0.6 mmol/L. PTHrP further significantly enhanced the low-Ca++–stimulated PTH secretion (P < 0.01, N = 6). Furthermore, PTHrP significantly enhanced (P < 0.008) the PTH secretion in the 1.35 mmol/L calcium-containing medium, but less as compared with the low-calcium medium (N = 5, mean ± SEM).
Kidney International  , 71-81DOI: ( /j x)
Copyright © 2000 International Society of Nephrology Terms and Conditions