Effect of chronic ethanol consumption on the response of parathyroid hormone to hypocalcemia in the pregnant rat.
BACKGROUND
Chronic alcohol (ethanol) consumption during pregnancy results in maternal/fetal hypocalcemia, which may underlie some of ethanol's adverse effects on maternal and fetal bone, and fetal/neonatal health. Ethanol appears to alter the relationship between parathyroid hormone (PTH) and blood calcium (Ca) level, and PTH does not increase in response to ethanol-induced hypocalcemia. However, it is not known whether ethanol actually prevents PTH from responding, or whether the ability to regulate blood Ca is intact, but ethanol lowers the level of Ca maintained. The objective of this study was to determine whether chronic ethanol consumption impairs the ability of the pregnant female to increase PTH in response to acute hypocalcemia.


METHODS
Rats were fed isocaloric diets with ethanol (36% ethanol-derived calories, E group) or without ethanol [pair-fed (PF) and control (C) groups], before and throughout 21 days of gestation. On day 21 gestation, rats received an intraperitoneal injection of ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) (300 or 500 mumol/kg body weight) or saline (saline group), or no injection (baseline group). Blood was collected from the baseline group, and at 30 or 60 minutes postinjection (saline and EGTA groups), and analyzed for ionized Ca (iCa), pH, and PTH.


RESULTS
Consistent with previous studies, ethanol consumption decreased blood iCa levels at baseline, but PTH levels did not differ among groups. Administration of EGTA significantly decreased blood iCa levels by 30 minutes, but ethanol did not prevent PTH from increasing in response to the hypocalcemia. In all diet groups, PTH levels were significantly increased by 30 minutes. Ethanol did, however, appear to decrease the maximum PTH level achievable in blood.


CONCLUSIONS
These data suggest that chronic ethanol consumption does not impair the ability of the pregnant rat to raise serum PTH levels in response to acute hypocalcemia, but ethanol's effect on maximal PTH secretion could impair the ability of the pregnant female to sustain high PTH levels in response to chronic hypocalcemia.
Duggal
Shalu
S
Food, Nutrition and Health, Faculty of Land and Food Systems, University of British Columbia, 2205 East Mall, Vancouver, British Columbia, Canada.
Simpson
Mary Elizabeth
ME
Keiver
Kathy
K
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002118:Calcium / Q000097:blood; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D002614:Chelating Agents / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood; D004533:Egtazic Acid / Q000494:pharmacology; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D006996:Hypocalcemia / Q000097:blood*; D017711:Nonlinear Dynamics; D010281:Parathyroid Hormone / Q000097:blood*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley
D002492:Central Nervous System Depressants; D002614:Chelating Agents; D010281:Parathyroid Hormone; D000431:Ethanol; D004533:Egtazic Acid; D002118:Calcium; D003345:Corticosterone