At the adrenergic junction of the sympathetic nerve with the medial smooth muscle of the cat nictitating membrane, blocking of the reuptake of noradrenaline with phenoxibenzamine suppressed the amplitude of rhythmic excitatory synaptic potentials. Stimulation of postganglionic sympathetic nerve (10/sec) made the time constant of the first component of the potential 60 sec whereas that of the second component--600 sec. The depression of amplitude seems to be connected with possible decrease in the noradrenaline release and partial exhaustion of its storage. The analysis of the transmitter function showed the release of noradrenaline to a single impulse to be in the reverse relation to the stimulation frequency and at 10/sec to constitute about 3 x 10(-4) (at 20/sec -1.9 X 10(-4)) of the transmitter storage. The replenishment of the transmitter (4 x 10(-6) of the initial operating pool of noradrenaline to a single impulse at 10/sec) was intensified parallel to the increased frequency of adrenergic neurons firing and was able to provide for afferent synaptic transmission within the working frequencies of the afferent part of the sympathetic reflex arch.
Download full-text PDF |
Source |
---|
Cardiol Rev
January 2025
Department of Internal Medicine, Milton S Hershey Medical Center, Hershey, PA.
Moyamoya disease (MMD) is a vascular disorder characterized by steno-occlusive alterations in cerebral arteries, often resulting in ischemic or hemorrhagic events predominantly affecting the female population and more common in Asian populations. Despite its predominantly neurological manifestations, recent research suggests a potential association between MMD and cardiovascular diseases (CVDs). MMD involves various genetic and environmental factors, with mutations in the RNF213 gene being strongly implicated in disease susceptibility, with histopathological findings revealing intimal lesions and smooth muscle proliferation, contributing to vascular occlusion as well as dysregulation of circulating endothelial and smooth muscle progenitor cells further complicating MMD's pathogenesis.
View Article and Find Full Text PDFRegen Ther
March 2025
Pediatric Urology and Regenerative Medicine Research Center, Gene Cell and Tissue Research Institute Children Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Tissue engineering has been considered a potential choice for urinary system reconstruction. Here, we aim to a broad spectrum of employed stem cells in bladder regeneration by performing a comprehensive systematic review. In January 2024, we searched Scopus, PubMed, and Embase databases for studies that tried bladder regeneration by tissue engineering using stem cells.
View Article and Find Full Text PDFJVS Vasc Sci
December 2024
Department of Cardiovascular Science, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile.
View Article and Find Full Text PDFEClinicalMedicine
January 2025
Department of Mathematics, University of Auckland, Auckland, New Zealand.
With the impending 'retirement' of bronchial thermoplasty (BT) for the treatment of patients with asthma, there is much to learn from this real-world experiment that will help us develop more effective future therapies with the same primary target i.e., airway smooth muscle (ASM) remodelling.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Shanghai Fifth People's Hospital and Institutes of Biomedical Sciences Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Loss-of-function mutations in NOTCH1 were previously linked to thoracic aortopathy, a condition for which non-surgical treatment options are limited. Based on clinical proteome analysis, we hypothesized that mitochondrial fusion and biogenesis in aortic smooth muscle cells (SMCs) are crucial for regulating the progression of NOTCH1-related aortopathy. Here we demonstrate that SMC-specific Notch1 knockout mice develop aortic pathology, including stiffening, dilation and focal dissection.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!