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Central infusion of a nitric oxide donor restores baroreflex control of heart rate in heart failure
Author(s) -
Ramchandra Rohit,
Hood Sally G,
May Clive N
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.24
Subject(s) - baroreflex , sodium nitroprusside , heart rate , medicine , heart failure , cardiology , nitric oxide synthase , anesthesia , cardiac output , blood pressure , nitric oxide
One of the hallmarks of heart failure (HF) is increased sympathetic nerve activity (SNA) to the heart and the kidney as well as depressed baroreflex control of heart rate (HR), but the mechanisms responsible remain unclear. We hypothesized that HF is associated with a reduction in central levels of NO synthase and that restoration of central NO levels in HF animals would be beneficial. Arterial pressure, HR, cardiac and renal SNA were recorded simultaneously in conscious sheep, at least 4 days after surgery in normal (n=7) and HF animals (n=7). HF was associated with a significant decrease in the levels of NO synthase in the brainstem (n=3). HF sheep had significant increases in baseline cardiac SNA levels and baroreflex control of HR was impaired. Intracerebroventricular (ICV) infusion of sodium nitroprusside (500 μg/ml/hr for 150 mins) led to a significant decrease in cardiac SNA in both normal (to 72 ± 10% of controland HF sheep (to 80± 6% of control. In addition there was a significant increase in the gain of baroreflex control of HR (from −2.28 ± 0.75 to −3.02 ± 10 bpm/mmHg, p<0.05), but there was no change in the normals. In contrast to cardiac SNA, there was no change in the baseline levels or baroreflex control of renal SNA in either group of animals. In conclusion, our data indicate an important role for NO in modulating baseline levels and baroreflex control of cardiac SNA.