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Expression of troponin subunits in the rat renal afferent arteriole
Author(s) -
Takeya Kosuke,
Kathol Iris,
Sutherland Cindy,
Wang Xuemei,
Loutzenhiser Rodger,
Walsh Michael P.
Publication year - 2019
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2061
Subject(s) - skeletal muscle , afferent arterioles , arteriole , medicine , endocrinology , myosin , gene isoform , troponin t , myogenic contraction , troponin , cardiac muscle , chemistry , biology , anatomy , microbiology and biotechnology , circulatory system , biochemistry , blood pressure , renin–angiotensin system , myocardial infarction , gene , smooth muscle
Vascular smooth muscle cells of the renal afferent arteriole are unusual in that they must be able to contract very rapidly in response to a sudden increase in systemic blood pressure in order to protect the downstream glomerular capillaries from catastrophic damage. We showed that this could be accounted for, in part, by exclusive expression, at the protein level, of the “fast” (B) isoforms of smooth muscle myosin II heavy chains in the afferent arteriole, in contrast to other vascular smooth muscle cells such as the rat aorta and efferent arteriole which express exclusively the “slow” (A) isoforms (Shiraishi et al. (2003) FASEB. J . 17 , 2284–2286). As contraction of the more rapidly contracting striated (skeletal and cardiac) muscles is regulated by the thin filament‐associated troponin (Tn) system, we hypothesized that Tn or a Tn‐like system may exist in afferent arteriolar cells and contribute to the unusually rapid contraction of this tissue in response to increased intraluminal pressure. We examined the expression of TnC (Ca 2+ ‐binding subunit), TnI (inhibitory subunit), and TnT (tropomyosin‐binding subunit) in vascular smooth muscle cells of the rat renal afferent arteriole at the mRNA level. Fast‐twitch skeletal muscle and slow‐twitch skeletal muscle/cardiac TnC isoforms and slow‐twitch skeletal muscle and cardiac TnI isoforms were detected by reverse transcription‐polymerase chain reaction (RT‐PCR) and confirmed by cDNA sequencing. Furthermore, cardiac and slow‐twitch skeletal muscle TnI isoforms, but not fast‐twitch skeletal muscle TnI, were detected in isolated afferent arterioles at the protein level by proximity ligation assay. Finally, striated muscle myosin II heavy chain expression was identified in isolated rat afferent arterioles by RT‐PCR. We conclude that, in addition to Ca 2+ ‐mediated phosphorylation of myosin II regulatory light chains, contraction of the afferent arteriole may be regulated by a mechanism normally associated with the much more rapidly contracting cardiac and skeletal muscles, which involves Ca 2+ binding to TnC, leading to alleviation of inhibition of the actomyosin MgATPase by TnI and tropomyosin and rapid contraction of the vessel.