Neuronal nitric oxide synthase modulation of intracellular Ca2+ handling overrides fatty acid potentiation of cardiac inotropy in hypertensive rats View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-05-22

AUTHORS

Chun Li Jin, Ming Zhe Yin, Jin Chul Paeng, Seunggyun Ha, Jeong Hoon Lee, Peng Jin, Chun Zi Jin, Zai Hao Zhao, Yue Wang, Keon Wook Kang, Chae Hun Leem, Jong-Wan Park, Sung Joon Kim, Yin Hua Zhang

ABSTRACT

Cardiac neuronal nitric oxide synthase (nNOS) is an important molecule that regulates intracellular Ca2+ homeostasis and contractility of healthy and diseased hearts. Here, we examined the effects of nNOS on fatty acid (FA) regulation of left ventricular (LV) myocyte contraction in sham and angiotensin II (Ang II)-induced hypertensive (HTN) rats. Our results showed that palmitic acid (PA, 100 μM) increased the amplitudes of sarcomere shortening and intracellular ATP in sham but not in HTN despite oxygen consumption rate (OCR) was increased by PA in both groups. Carnitine palmitoyltransferase-1 inhibitor, etomoxir (ETO), reduced OCR and ATP with PA in sham and HTN but prevented PA potentiation of sarcomere shortening only in sham. PA increased nNOS-derived NO only in HTN. Inhibition of nNOS with S-methyl-l-thiocitrulline (SMTC) prevented PA-induced OCR and restored PA potentiation of myocyte contraction in HTN. Mechanistically, PA increased intracellular Ca2+ transient ([Ca2+]i) without changing Ca2+ influx via L-type Ca2+ channel (I-LTCC) and reduced myofilament Ca2+ sensitivity in sham. nNOS inhibition increased [Ca2+]i, I-LTCC and reduced myofilament Ca2+ sensitivity prior to PA supplementation; as such, normalized PA increment of [Ca2+]i. In HTN, PA reduced I-LTCC without affecting [Ca2+]i or myofilament Ca2+ sensitivity. However, PA increased I-LTCC, [Ca2+]i and reduced myofilament Ca2+ sensitivity following nNOS inhibition. Myocardial FA oxidation (18F-fluoro-6-thia-heptadecanoic acid, 18F-FTHA) was comparable between groups, but nNOS inhibition increased it only in HTN. Collectively, PA increases myocyte contraction through stimulating [Ca2+]i and mitochondrial activity in healthy hearts. PA-dependent cardiac inotropy was limited by nNOS in HTN, predominantly due to its modulatory effect on [Ca2+]i handling. More... »

PAGES

1359-1371

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00424-017-1991-1

DOI

http://dx.doi.org/10.1007/s00424-017-1991-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1085568228

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28534086


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22 schema:description Cardiac neuronal nitric oxide synthase (nNOS) is an important molecule that regulates intracellular Ca2+ homeostasis and contractility of healthy and diseased hearts. Here, we examined the effects of nNOS on fatty acid (FA) regulation of left ventricular (LV) myocyte contraction in sham and angiotensin II (Ang II)-induced hypertensive (HTN) rats. Our results showed that palmitic acid (PA, 100 μM) increased the amplitudes of sarcomere shortening and intracellular ATP in sham but not in HTN despite oxygen consumption rate (OCR) was increased by PA in both groups. Carnitine palmitoyltransferase-1 inhibitor, etomoxir (ETO), reduced OCR and ATP with PA in sham and HTN but prevented PA potentiation of sarcomere shortening only in sham. PA increased nNOS-derived NO only in HTN. Inhibition of nNOS with S-methyl-l-thiocitrulline (SMTC) prevented PA-induced OCR and restored PA potentiation of myocyte contraction in HTN. Mechanistically, PA increased intracellular Ca2+ transient ([Ca2+]i) without changing Ca2+ influx via L-type Ca2+ channel (I-LTCC) and reduced myofilament Ca2+ sensitivity in sham. nNOS inhibition increased [Ca2+]i, I-LTCC and reduced myofilament Ca2+ sensitivity prior to PA supplementation; as such, normalized PA increment of [Ca2+]i. In HTN, PA reduced I-LTCC without affecting [Ca2+]i or myofilament Ca2+ sensitivity. However, PA increased I-LTCC, [Ca2+]i and reduced myofilament Ca2+ sensitivity following nNOS inhibition. Myocardial FA oxidation (18F-fluoro-6-thia-heptadecanoic acid, 18F-FTHA) was comparable between groups, but nNOS inhibition increased it only in HTN. Collectively, PA increases myocyte contraction through stimulating [Ca2+]i and mitochondrial activity in healthy hearts. PA-dependent cardiac inotropy was limited by nNOS in HTN, predominantly due to its modulatory effect on [Ca2+]i handling.
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28 schema:keywords ATP
29 Ang
30 Ca2
31 FA oxidation
32 HTN
33 L-type Ca2
34 Mechanistically
35 PA
36 PA increment
37 PA supplementation
38 S-methyl
39 acid
40 acid regulation
41 activity
42 amplitude
43 angiotensin II
44 cardiac inotropy
45 carnitine palmitoyltransferase-1 inhibitor
46 channels
47 consumption rate
48 contractility
49 contraction
50 diseased heart
51 effect
52 etomoxir
53 fatty acid potentiation
54 fatty acid regulation
55 group
56 handling
57 healthy heart
58 heart
59 homeostasis
60 hypertensive rats
61 important molecules
62 increment
63 influx
64 inhibition
65 inhibition of nNOS
66 inhibitors
67 inotropy
68 intracellular Ca2
69 mitochondrial activity
70 modulation
71 modulatory effects
72 molecules
73 myocardial FA oxidation
74 myocyte contraction
75 myofilament Ca2
76 nNOS inhibition
77 neuronal nitric oxide synthase
78 nitric oxide synthase
79 oxidation
80 oxide synthase
81 oxygen consumption rate
82 palmitic acid
83 potentiation
84 rate
85 rats
86 regulation
87 results
88 sarcomere shortening
89 sarcomeres
90 sensitivity
91 sham
92 shortening
93 supplementation
94 synthase
95 thiocitrulline
96 transients
97 ventricular myocyte contraction
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