Substance P in heart failure: The good and the bad

Dehlin, Heather M.; Levick, Scott P.

doi:10.1016/j.ijcard.2013.11.010

Cited by 62 publications

(51 citation statements)

References 79 publications

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“…Normalized sympathetic and parasympathetic activity implies inhibition of catecholamine toxicity at the source rather than blockade at the end-organ level, thereby inhibiting release of other neurotransmitters including substance P and neuropeptide Y that may contribute to disease progression [14,15]. Moreover, the inhibitory effects of vagal activation on proinflammatory interleukins are well documented [16].…”

Section: Discussionmentioning

confidence: 99%

Long-term chronic baroreflex activation

Gronda

Seravalle

Trevano

et al. 2015

Journal of Hypertension

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Aims: Baroreflex activation therapy (BAT) has recently been shown to reduce muscle sympathetic nerve activity and hospitalization rate while improving clinical variables through 6 months of therapy in patients with heart failure and reduced ejection fraction (HFrEF). The objective of the present study is to extend the information on this patient cohort over a long-term follow-up.Methods and results: Eleven patients were enrolled in the study and presented with optimized, stable medical therapy, New York Heart Association Class III HFrEF with left ventricular ejection fraction 40% or less, impaired functional capacity and no active cardiac resynchronization therapy. For the present report, muscle sympathetic nerve activity, baroreflex sensitivity data and hospitalization rate together with standard clinical data were collected at 12 and 21.5 AE 4.2 months following BAT activation. Two patients died during long-term follow-up. The remaining nine patients maintained the improvements observed at 6 months, including reduced sympathetic activity and rates of hospitalization.Conclusion: BAT provides long-term chronic reductions in sympathetic activity and utilization of hospital resources in patients with HFrEF. General clinical presentation, quality of life and functional capacity are likewise improved and maintained. The temporal association of BAT with sympathetic drive diminution and improvement in objective clinical measures suggests a cause-and-effect relationship that will be verified in future randomized controlled trials of outcome.

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Section: Discussionmentioning

confidence: 99%

Long-term chronic baroreflex activation

Gronda

Seravalle

Trevano

et al. 2015

Journal of Hypertension

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“…Jest to generalnie zgodne z wcześniejszymi obserwacjami dotyczącymi włókien zlokalizowanych w innych częściach serca, takich jak przegroda lub ściany przedsionków i komór (31,35,45), w których (podobnie jak podczas niniejszych badań) obserwowano NPY, VAChT, TH oraz SP (8,9,45). Z drugiej jednak strony, zauważyć można pewne różnice pomiędzy neurochemiczną charakterystyką włókien nerwowych zaopatrujących koniuszek serca (wyniki niniejszych badań) a strukturami nerwowymi w innych częściach serca opisanymi we wcześniejszych eksperymentach (31).…”

Section: Cgrp)unclassified

“…Ponadto SP uczestniczy w regulacji przepływu krwi przez naczynia wieńcowe (21,35) oraz pobudza unerwienie cholinergiczne serca, powodując ujemny efekt ino-, batmo-i chronotropowy (11). W warunkach eksperymentalnych SP może oddziaływać stymulująco na wzrost i rozwój kardiomiocytów (9).…”

Section: Cgrp)unclassified

Influence of bisfenol A on chemical coding of the nerve fibers of the cardiac apex in the domestic pig

Makowska

Szymańska

Palus

et al. 2017

Medycyna Weterynaryjna

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“…Animal ischaemia reperfusion studies show that substance P having a protective effect by increasing coronary perfusion and attenuating hypoxic cellular damage 34. However chronic exposure to substance P induces inflammation, apoptosis and matrix metalloproteinase activation which result in adverse remodelling 34…”

Section: Sacubitril/valsartan and Its Effects On Other Peptide Hormonesmentioning

confidence: 99%

Sacubitril/valsartan: beyond natriuretic peptides

Singh

Burrell

Cherif

et al. 2017

Heart

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Natriuretic peptides, especially B-type natriuretic peptide (BNP), have primarily been regarded as biomarkers in heart failure (HF). However, they are also possible therapeutic agents due to potentially beneficial physiological effects.The angiotensin receptor-neprilysin inhibitor (ARNI), sacubitril/valsartan, simultaneously augments the natriuretic peptide system (NPS) by inhibiting the enzyme neprilysin (NEP) and inhibits the renin-angiotensin-aldosterone system First we discuss how NPS physiology differs between healthy individuals and those with HF by looking at mechanisms like the overwhelming effects of RAAS on the NPS, natriuretic peptide receptor desensitisation and absolute natriuretic deficiency. Secondly, this review explores other hormones that are augmented by sacubitril/valsartan such as, bradykinin, substance-P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF. We also discuss concerns that sacubitril/valsartan may interfere with amyloid β homeostasis with potential implications on Alzheimer's disease and macular degeneration. Finally, we explore the concept of 'auto-inhibition' which is a recently described observation that humans have innate NEP inhibitory capability when natriuretic peptide levels rise above a threshold. There is speculation that auto-inhibition may provide a surge of natriuretic and other vasoactive peptides to rapidly reverse decompensation. We contend that by pre-emptively inhibiting NEP, sacubitril/valsartan is inducing this surge earlier during decompensation, resulting in the better outcomes observed.

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Substance P in heart failure: The good and the bad

Cited by 62 publications

References 79 publications

Long-term chronic baroreflex activation

Long-term chronic baroreflex activation

Influence of bisfenol A on chemical coding of the nerve fibers of the cardiac apex in the domestic pig

Sacubitril/valsartan: beyond natriuretic peptides

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