PMID- 8783675
OWN - NLM
STAT- MEDLINE
DCOM- 19961017
LR  - 20131121
IS  - 0002-9629 (Print)
IS  - 0002-9629 (Linking)
VI  - 312
IP  - 3
DP  - 1996 Sep
TI  - The First Annual Bayard D. Catherwood Memorial Lecture. Ca2+-receptor-mediated 
      regulation of parathyroid and renal function.
PG  - 99-109
AB  - The recent cloning of an extracellular calcium (Ca2+o)-sensing receptor (CaR) 
      from the parathyroid gland and the kidney has provided novel insights into the 
      mechanisms that underlie the direct actions of Ca2+o on various cells. The 
      receptor is a member of the superfamily of G protein-coupled receptors, 
      activating phospholipase C (PLC) and probably also inhibiting adenylate cyclase 
      in target tissues. In the parathyroid gland it is a key mediator of the 
      inhibition by high Ca2+o of parathyroid hormone (PTH) secretion and, perhaps, PTH 
      gene expression and parathyroid cellular proliferation. It also appears to 
      represent the major mechanism through which Ca2+o stimulates the secretion of 
      calcitonin from the thyroidal C-cells. In the kidney, the CaR directly inhibits 
      tubular reabsorption of calcium and magnesium in the thick ascending limb, and 
      may be responsible for the long-recognized, but poorly understood inhibition of 
      urinary concentrating ability by hypercalcemia. The demonstration that activating 
      and inactivating mutations of the CaR, respectively, are the proximate causes of 
      the inherited hypocalcemic disorder, autosomal dominant hypocalcemia (ADH) and 
      the hypercalcemic diseases, familial hypocalciuric hypercalcemia (FHH) and 
      neonatal severe hyperparathyroidism (NSHPT), has provided additional strong 
      support for the physiologic importance of the CaR in human mineral ion 
      homeostasis. Therefore, when Ca2+o acts through its own G protein-coupled cell 
      surface receptor, it acts as an extracellular first messenger in addition to 
      serving its better recognized role as a key intracellular second messenger.
FAU - Brown, E M
AU  - Brown EM
AD  - Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 
      Boston, Massachusetts, USA.
FAU - Hebert, S C
AU  - Hebert SC
LA  - eng
GR  - DK41415/DK/NIDDK NIH HHS/United States
GR  - DK44588/DK/NIDDK NIH HHS/United States
GR  - DK46422/DK/NIDDK NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Am J Med Sci
JT  - The American journal of the medical sciences
JID - 0370506
RN  - 0 (Receptors, Calcium-Sensing)
RN  - 0 (Receptors, Cell Surface)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Cattle
MH  - Humans
MH  - Hypercalcemia/etiology
MH  - Hypocalcemia/etiology
MH  - Kidney/*physiology
MH  - Mice
MH  - Parathyroid Glands/*physiology
MH  - Receptors, Calcium-Sensing
MH  - Receptors, Cell Surface/*physiology
MH  - Signal Transduction
RF  - 69
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - S0002-9629(15)41773-2 [pii]
PST - ppublish
SO  - Am J Med Sci. 1996 Sep;312(3):99-109.