Substance P and beta-endorphin levels in the plasma and pericardial fluid in patients with and without angina

Kambam, J. R.; Parris, W; Merrill, Walter H.; Naukam, Rebecca; Sastry, B. V. Rama

doi:10.1016/0304-3959(90)93025-s

Cited by 5 publications

(5 citation statements)

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“…Certainly support of a role for substance P can be found in humans, where plasma levels are elevated in patients with congestive heart failure (NYHA class I-IV) (75). Also, Kambam et al (76) found that patients with angina pectoris had higher levels of substance P than patients without angina, however, they could only detect substance P in pericardial fluid and not plasma, indicating that in some instances plasma may not be a good marker of substance P due to its localized release. The targeting of substance P is very exciting, however, it is early days and many more studies both in animals and humans are needed to fine tune this concept.…”

Section: 0 Clinical Implicationsmentioning

confidence: 99%

Substance P in heart failure: The good and the bad

Dehlin¹,

Levick²

2014

International Journal of Cardiology

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The tachykinin, substance P, is found primarily in sensory nerves. In the heart, substance P-containing nerve fibers are often found surrounding coronary vessels, making them ideally situated to sense changes in the myocardial environment. Recent studies in rodents have identified substance P as having dual roles in the heart, depending on disease etiology and/or timing. Thus far, these studies indicate that substance P may be protective acutely following ischemia-reperfusion, but damaging long-term in non-ischemic induced remodeling and heart failure. Sensory nerves may be at the apex of the cascade of events leading to heart failure, therefore, they make a promising potential therapeutic target that warrants increased investigation.

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Section: 0 Clinical Implicationsmentioning

confidence: 99%

Substance P in heart failure: The good and the bad

Dehlin¹,

Levick²

2014

International Journal of Cardiology

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“…If one extrapolates this finding to humans, it may mean that humans are more sensitive to the adverse effects of SP in disease. Increased levels of SP have been detected in heart failure patients [33], patients with angina pectoris [14], and in atherosclerotic lesions of human coronary arteries [18]. Overall, this study demonstrates that rat fibroblasts respond similarly to non-human primate cells, which makes rodent fibroblasts a suitable model to study fibroblast responses to SP in the absence of non-human primate cells.…”

Section: Discussionmentioning

confidence: 71%

Non-human Primate and Rat Cardiac Fibroblasts Show Similar Extracellular Matrix-related and Cellular Adhesion Gene Responses to Substance P

Meléndez

Manteufel

Dehlin

et al. 2015

Heart, Lung and Circulation

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Background The sensory nerve neuropeptide substance P (SP) regulates cardiac fibrosis in rodents under pressure overload conditions. Interestingly, SP induces transient increase expression of specific genes in isolated rat cardiac fibroblasts, without resultant changes in cell function. This suggests that SP ‘primes’ fibroblasts, but does not directly activate them. We investigated whether these unusual findings are specific to rodent fibroblasts or are translatable to a larger animal model more closely related to humans. Methods We compared the effects of SP on genes associated with extracellular matrix (ECM) regulation, cell-cell adhesion, cell-matrix adhesion and ECM in cardiac fibroblasts isolated from a non-human primate and Sprague-Dawley rats. Results We found that rodent and non-human primate cardiac fibroblasts showed similar ECM regulation and cell adhesion gene expression responses to SP. There were, however, large discrepancies in ECM genes which did not result in collagen or laminin synthesis in rat or non-human primate fibroblasts in response to SP. Conclusions This study further supports the notion that SP serves as a ‘primer’ for fibroblasts rather than initiating direct effects and suggests that rodent fibroblasts are a suitable model for studying gene and functional responses to SP in the absence of human or non-human primate fibroblasts.

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“…It appears that endogenous opiates can also be released from the human heart. BE, met-enkephalin, leu-enkephalin, and dynorphin have been detected in human coronary sinus blood (25), and BE has been observed in the pericardial fluid (26). In addition, BE in the coronary sinus blood tended to be increased by epidural spinal electrical stimulation in patients with coronary artery disease in which angina was induced by atrial pacing (25).…”

Section: Stress and Be In The Rat Heartmentioning

confidence: 97%

The Results of Exposure to Immobilization, Hemorrhagic Shock, and Cardiac Hypertrophy on -Endorphin in Rat Cardiac Tissue

Forman

Hock

Harwell

et al. 1994

Experimental Biology and Medicine

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In the present study, beta-endorphin (BE), beta-lipotropin (B-LPH) and the ratio of beta-endorphin to beta-lipotropin (BE:B-LPH) were determined in rat cardiac tissue in response to physical stress induced by immobilization and cardiovascular stress resulting from hemorrhagic shock and pressure overload-induced cardiac hypertrophy. As compared with controls, BE was increased and B-LPH was decreased in cardiac tissue from animals subjected to immobilization, and there was also a significant rise in the ratio of BE:B-LPH. Cardiac BE remained unchanged following hemorrhage, while B-LPH was diminished, resulting in an increase in the ratio of BE:B-LPH. Similarly, the concentration of BE was unchanged, the concentration of B-LPH was significantly diminished and the ratio of BE:B-LPH was significantly increased in hypertrophied hearts. Thus, immobilization-induced stress, hemorrhagic shock, and cardiac hypertrophy all increased the ratio of BE:B-LPH in the heart. However, it appears that immobilization stress induces an increase in cardiac BE, whereas cardiovascular stress results in a preservation of BE in the heart and a reduction in cardiac B-LPH. The data suggests that physical stress (induced by immobilization) and cardiovascular stress (i.e., hemorrhage, hypertrophy) have differential effects on the synthesis of BE and the post-translational processing of proopiomelanocortin in the heart. Furthermore, the alterations in cardiac tissue BE and possibly B-LPH may play a role in the response of the heart to physical and cardiovascular stress.

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Substance P and beta-endorphin levels in the plasma and pericardial fluid in patients with and without angina

Cited by 5 publications

References 0 publications

Substance P in heart failure: The good and the bad

Substance P in heart failure: The good and the bad

Non-human Primate and Rat Cardiac Fibroblasts Show Similar Extracellular Matrix-related and Cellular Adhesion Gene Responses to Substance P

The Results of Exposure to Immobilization, Hemorrhagic Shock, and Cardiac Hypertrophy on -Endorphin in Rat Cardiac Tissue

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