PMID- 15817832
OWN - NLM
STAT- MEDLINE
DCOM- 20050517
LR  - 20220409
IS  - 0022-0795 (Print)
IS  - 0022-0795 (Linking)
VI  - 185
IP  - 1
DP  - 2005 Apr
TI  - Thyroid status and nitric oxide in rat arterial vessels.
PG  - 111-9
AB  - Thyroid disease has profound effects on cardiovascular function. Hypo- and 
      hyperthyroidism, for example, are associated with reduced and increased maximal 
      endothelium-dependent vasodilation respectively. We therefore hypothesized that 
      the capacity for vascular nitric oxide (NO) formation is decreased in 
      hypothyroidism and increased in hyperthyroidism. To test this hypothesis, rats 
      were made hypothyroid (HYPO) with propylthiouracil or hyperthyroid (HYPER) with 
      triiodothyronine over 3-4 months. Compared with euthyroid control rats (EUT), 
      HYPO exhibited blunted growth and lower citrate synthase activity in the soleus 
      muscle; HYPER exhibited left ventricular hypertrophy and higher citrate synthase 
      activity in the soleus muscle (P<0.05 for all effects). The capacity for NO 
      formation was determined in aortic extracts by formation of [3H]L-citrulline from 
      [3H]L-arginine, i.e. NO synthase (NOS) activity. Thyroid status modulated NOS 
      activity (EUT, 36.8 +/- 5.5 fmol/h per mg protein; HYPO, 26.0 +/- 7.9; HYPER, 
      64.6 +/- 12.7; P<0.05, HYPER vs HYPO). Expression of endothelial and neural 
      isoforms of NOS was modulated by thyroid status in a parallel fashion. Capacity 
      for responding to NO was also determined via measuring cGMP concentration in 
      aortae incubated with sodium nitroprusside. Stimulated cGMP formation was also 
      modulated by thyroid status (EUT, 73.0 +/- 20.2 pmol/mg protein; HYPO, 152.4 +/- 
      48.7; HYPER, 10.4 +/- 2.6; P<0.05, HYPER vs HYPO). These data indicate that 
      thyroid status alters capacities for both formation of and responding to NO. The 
      former finding may contribute to previous findings concerning vascular function 
      in thyroid disease states.
FAU - McAllister, R M
AU  - McAllister RM
AD  - Department of Anatomy and Physiology and Kinesiology, Kansas State University, 
      Manhattan, Kansas 66506, USA. mcallist@vet.ksu.edu
FAU - Albarracin, I
AU  - Albarracin I
FAU - Price, E M
AU  - Price EM
FAU - Smith, T K
AU  - Smith TK
FAU - Turk, J R
AU  - Turk JR
FAU - Wyatt, K D
AU  - Wyatt KD
LA  - eng
GR  - HL 57226/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (Vasodilator Agents)
RN  - 169D1260KM (Nitroprusside)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 2.3.3.1 (Citrate (si)-Synthase)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Animals
MH  - Aorta
MH  - Citrate (si)-Synthase/metabolism
MH  - Cyclic GMP/metabolism
MH  - Endothelium, Vascular/*metabolism
MH  - Hyperthyroidism/metabolism
MH  - Hypothyroidism/metabolism
MH  - Immunohistochemistry/methods
MH  - Male
MH  - Muscle, Skeletal/enzymology
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Nitroprusside/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Thyroid Diseases/*metabolism
MH  - Vasodilator Agents/pharmacology
EDAT- 2005/04/09 09:00
MHDA- 2005/05/18 09:00
CRDT- 2005/04/09 09:00
PHST- 2005/04/09 09:00 [pubmed]
PHST- 2005/05/18 09:00 [medline]
PHST- 2005/04/09 09:00 [entrez]
AID - 185/1/111 [pii]
AID - 10.1677/joe.1.06022 [doi]
PST - ppublish
SO  - J Endocrinol. 2005 Apr;185(1):111-9. doi: 10.1677/joe.1.06022.