{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T21:18:11Z","timestamp":1780435091818,"version":"3.54.1"},"reference-count":69,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health","doi-asserted-by":"publisher","award":["P01 HL70687"],"award-info":[{"award-number":["P01 HL70687"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL122223"],"award-info":[{"award-number":["R01 HL122223"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2020,2,1]]},"abstract":"<jats:p> Complications associated with spinal cord injury (SCI) result from unregulated reflexes below the lesion level. Understanding neurotransmission distal to the SCI could improve quality of life by mitigating complications. The long-term impact of SCI on neurovascular transmission is poorly understood, but reduced sympathetic activity below the site of SCI enhances arterial neurotransmission (1). We studied sympathetic neurovascular transmission using a rat model of long-term paraplegia (T2\u20133) and tetraplegia (C6\u20137). Sixteen weeks after SCI, T2\u20133 and C6\u20137 rats had lower blood pressure (BP) than sham rats (103\u2009 \u00b1 \u20092 and 97\u2009 \u00b1\u2009 4 vs. 117\u2009 \u00b1 \u20096 mmHg, P &lt; 0.05). T2\u20133 rats had tachycardia (410\u2009 \u00b1 \u20096 beats\/min), and C6\u20137 rats had bradycardia (299\u2009 \u00b1\u2009 10 beats\/min) compared with intact rats (321\u2009 \u00b1\u2009 4 beats\/min, P &lt; 0.05). Purinergic excitatory junction potentials (EJPs) were measured in mesenteric arteries (MA) using microlectrodes, and norepinephrine (NE) release was measured using amperometry. NE release was similar in all groups, while EJP frequency-response curves from T2\u20133 and C6\u20137 rats were left-shifted vs. sham rats. EJPs in T2\u20133 and C6\u20137 rats showed facilitation followed by run-down during stimulation trains (10 Hz, 50 stimuli). MA reactivity to exogenous NE and ATP was similar in all rats. In T2\u20133 and C6\u20137 rats, NE content was increased in left cardiac ventricles compared with intact rats, but was not changed in MA, kidney, or spleen. Our data indicate that peripheral purinergic, but not adrenergic, neurotransmission increases following SCI via enhanced ATP release from periarterial nerves. Sympathetic BP support is reduced after SCI, but improving neurotransmitter release might maintain cardiovascular stability in individuals living with SCI. <\/jats:p><jats:p> NEW &amp; NOTEWORTHY This study revealed increased purinergic, but not noradrenergic, neurotransmission to mesenteric arteries in rats with spinal cord injury (SCI). An increased releasable pool of ATP in periarterial sympathetic nerves may contribute to autonomic dysreflexia following SCI, suggesting that purinergic neurotransmission may be a therapeutic target for maintaining stable blood pressure in individuals living with SCI. The selective increase in ATP release suggests that ATP and norepinephrine may be stored in separate synaptic vesicles in periarterial sympathetic varicosities. <\/jats:p>","DOI":"10.1152\/ajpheart.00525.2019","type":"journal-article","created":{"date-parts":[[2019,11,27]],"date-time":"2019-11-27T13:54:22Z","timestamp":1574862862000},"page":"H223-H237","source":"Crossref","is-referenced-by-count":7,"title":["Spinal cord injury alters purinergic neurotransmission to mesenteric arteries in rats"],"prefix":"10.1152","volume":"318","author":[{"given":"Sutheera","family":"Sangsiri","sequence":"first","affiliation":[{"name":"Department of Preclinical Science, Thammasat University, Pathumthani, Thailand"},{"name":"Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Michigan State 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