PMID- 9518867
OWN - NLM
STAT- MEDLINE
DCOM- 19980403
LR  - 20190709
IS  - 0022-0795 (Print)
IS  - 0022-0795 (Linking)
VI  - 156
IP  - 2
DP  - 1998 Feb
TI  - Calcium blood level modulates endogenous nitric oxide action: effects of 
      parathroidectomy in patients with hyperparathyroidism.
PG  - 231-5
AB  - Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate 
      cyclase (sGC), the activity of which is modulated by the activity of nitric oxide 
      (NO) constitutive synthase (cNOS) which, in turn, is activated by a 
      calcium/calmodulin complex. In primary hyperparathyroidism (H-PTH) an increase in 
      platelet free calcium levels is present. In this study we evaluate the platelet 
      cGMP levels, as an expression of NO production, in the presence of 
      3-isobutyl-1-methylxanthine (IBMX) alone (IBMXcGMP) and after stimulation by 
      ionomycine (IONO; IONOcGMP) and sodium nitroprusside (SNP; SNPcGMP), in eight 
      subjects affected by H-PTH before and after removal of adenoma. Platelet cGMP 
      levels were also measured in seven normal subjects. IBMXcGMP and IONOcGMP were 
      elevated in H-PTH patients compared with normal subjects (1.9 +/- 0.3 vs 0.8 +/- 
      0.2 fmol/10(6) platelets and 2.7 +/- 0.4 vs 1.4 +/- 0.3; P < 0.02 and P < 0.05 
      respectively) but SNPcGMP was unaffected (3.9 +/- 0.6 vs 2.5 +/- 0.5). After 
      parathyroidectomy, blood levels of intact parathyroid hormone (i-PTH), total 
      calcium (t-Ca), IBMXcGMP and IONOcGMP all decreased (177.5 +/- 23.9 vs 45.0 +/- 
      8.8 pg/ml, P < 0.005; 6.5 +/- 0.5 vs 4.6 +/- 0.1 mEq/1, P < 0.005; 1.9 +/- 0.3 vs 
      0.8 +/- 0.2, P < 0.005; 2.7 +/- 0.4 vs 1.8 +/ 0.3, P < 0.05 respectively), while 
      SNPcGMP was not modified (3.9 +/- 0.6 vs 4.3 +/- 0.9). t-Ca and i-PTH were 
      directly correlated with IBMXcGMP (P < 0.02, rs = 0.613; P < 0.02, rs = 0.576 
      respectively) and i-PTH was also correlated with t-Ca (P < 0.001), rs = 0.840). 
      IN CONCLUSION: (1) levels of IBMXcGMP and IONOcGMP are high in subjects with 
      H-PTH; (2) after surgery both IBMXcGMP and IONOcGMP decrease to normal values. As 
      IBMXcGMP expresses basal cGMP and IONOcGMP expresses the cGMP after cNOS 
      stimulation, it can be speculated that the increase in NO production could be a 
      mechanism to downregulate the vasoconstriction which may be caused by the high 
      calcium levels in smooth muscle cells. After surgery, together with the 
      normalization of calcium levels, NO production also returned to normal values.
FAU - Martina, V
AU  - Martina V
AD  - Dipartimento di Medicina Interna, Universita degli Studi di Torino, Ospedale 
      Molinette, Italy.
FAU - Bruno, G A
AU  - Bruno GA
FAU - Brancaleoni, V
AU  - Brancaleoni V
FAU - Zumpano, E
AU  - Zumpano E
FAU - Tagliabue, M
AU  - Tagliabue M
FAU - Fornengo, R
AU  - Fornengo R
FAU - Gasparri, G
AU  - Gasparri G
FAU - Pescarmona, G P
AU  - Pescarmona GP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (Ionophores)
RN  - 0 (Phosphodiesterase Inhibitors)
RN  - 0 (Vasodilator Agents)
RN  - 169D1260KM (Nitroprusside)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 56092-81-0 (Ionomycin)
RN  - H2D2X058MU (Cyclic GMP)
RN  - SY7Q814VUP (Calcium)
RN  - TBT296U68M (1-Methyl-3-isobutylxanthine)
SB  - IM
MH  - 1-Methyl-3-isobutylxanthine/pharmacology
MH  - Adenoma/blood/complications/surgery
MH  - Blood Platelets/drug effects/metabolism
MH  - Calcium/*blood
MH  - Cyclic GMP/metabolism
MH  - Female
MH  - Humans
MH  - Hyperparathyroidism/etiology/*metabolism/surgery
MH  - In Vitro Techniques
MH  - Ionomycin/pharmacology
MH  - Ionophores/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Nitric Oxide/*metabolism
MH  - Nitroprusside/pharmacology
MH  - Parathyroid Neoplasms/blood/complications/surgery
MH  - Parathyroidectomy
MH  - Phosphodiesterase Inhibitors/pharmacology
MH  - Postoperative Period
MH  - Stimulation, Chemical
MH  - Vasodilator Agents/pharmacology
EDAT- 1998/03/31 00:00
MHDA- 1998/03/31 00:01
CRDT- 1998/03/31 00:00
PHST- 1998/03/31 00:00 [pubmed]
PHST- 1998/03/31 00:01 [medline]
PHST- 1998/03/31 00:00 [entrez]
AID - 10.1677/joe.0.1560231 [doi]
PST - ppublish
SO  - J Endocrinol. 1998 Feb;156(2):231-5. doi: 10.1677/joe.0.1560231.