Page 379 - Feline Cardiology

Chapter 26: Endocrine Diseases 397

Ca 2+ Triiodothyronine

Sarcoplasmic Cell
reticulum membrane

Ca 2+ Phospholamban
Nucleus

Ca 2+ Ca 2+ -
Ca 2+ - ATPase Thyroid
hormone
response
element
Triiodothyronine
Actin Myosin nuclear
mRNA
receptor
Cyclic AMP
Ca 2+

Protein
synthesis

Guanine-nucleotide–
binding protein

K +
Na +
Ca 2+

K + Adenylyl
cyclase b-Adrenergic
+
+
Na + Na /K – Voltage- receptor
ATPase +
+
Na /Ca 2+ gated K
exchanger channel
Triiodothyronine Endocrine Diseases
Figure 26.1. Intracellular actions of thyroid hormone. Reproduced with permission from the New England Journal of Medicine. Copy-
right 2001, Massachusetts Medical Society.

heavy chain predominates, making up more than 70% trast to the general documentation of hyperfunctional
of a euthyroid rat’s cardiac myosin, for example. but not prominently hypertrophied ventricles in human
Conversely, the human heart contains mainly β-myosin hyperthyroidism (Klein and Ojamaa 2001; Klein 2008).
heavy chain and the α-myosin heavy chain (V1) com- As will be discussed below, an alternative explanation
prises only 2.5% of cardiac myosin (Klein and Ojamaa could be the late recognition, with very dramatic lesions,
2001; Dillman 2002). Accordingly, in human hyperthy- of hyperthyroid patients in initial feline reports from the
roidism, few if any changes in expression of these cardiac early 1980s; by contrast, earlier recognition of hyperthy-
myosin isoforms is noted as compared to euthyroid roidism in cats at the present time coincides with very
humans (Klein 2008). Such interspecies differences may modest cardiac structural changes in these cats, as in
help to explain the routine occurrence of concentric humans. Finally, additional factors exist in hyperthy-
myocardial hypertrophy in hyperthyroid cats, in con- roidism that are likely to further contribute to left