Nitric Oxide Regulation of Myocardial Contractility and Calcium Cycling: Independent Impact of Neuronal and Endothelial Nitric Oxide Synthases

ABSTRACT—The mechanisms by which nitric oxide (NO) influences myocardial Ca cycling remain controversial. Because NO synthases (NOS) have specific spatial localization in cardiac myocytes, we hypothesized that neuronal NOS (NOS1) found in cardiac sarcoplasmic reticulum (SR) preferentially regulates...

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Veröffentlicht in:	Circulation research 2003-06, Vol.92 (12), p.1322-1329
Hauptverfasser:	Khan, Shakil A, Skaf, Michel W, Harrison, Robert W, Lee, Kwangho, Minhas, Khalid M, Kumar, Anil, Fradley, Mike, Shoukas, Artin A, Berkowitz, Dan E, Hare, Joshua M
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Blood Pressure - physiology Blotting, Western Calcium - metabolism Cell Size - physiology Electric Stimulation Female Fundamental and applied biological sciences. Psychology Genotype Heart Hemodynamics - physiology Male Mice Mice, Inbred C57BL Mice, Inbred Strains Mice, Knockout Muscle Proteins - metabolism Myocardial Contraction - physiology Myocytes, Cardiac - cytology Myocytes, Cardiac - metabolism Nitric Oxide - physiology Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type I Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Sarcomeres - physiology Sarcoplasmic Reticulum - metabolism Space life sciences Ventricular Function, Left - physiology Vertebrates: cardiovascular system
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Zusammenfassung:	ABSTRACT—The mechanisms by which nitric oxide (NO) influences myocardial Ca cycling remain controversial. Because NO synthases (NOS) have specific spatial localization in cardiac myocytes, we hypothesized that neuronal NOS (NOS1) found in cardiac sarcoplasmic reticulum (SR) preferentially regulates SR Ca release and reuptake resulting in potentiation of the cardiac force-frequency response (FFR). Transesophageal pacing (660 to 840 bpm) in intact C57Bl/6 mice (WT) stimulated both contractility (dP/dtmax normalized to end-diastolic volume; dP/dt-EDV) by 51±5% (P
ISSN:	0009-7330 1524-4571
DOI:	10.1161/01.RES.0000078171.52542.9E