{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T18:47:57Z","timestamp":1774464477184,"version":"3.50.1"},"reference-count":50,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2013,4,30]],"date-time":"2013-04-30T00:00:00Z","timestamp":1367280000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Key points<\/jats:title>\n                  <jats:p>\n                    <jats:list list-type=\"explicit-label\">\n                      <jats:list-item>\n                        <jats:p>To test whether the responses of the normal rat tail artery to supramaximal nerve stimulation depend on activating all of its innervation, half the sympathetic innervation was surgically removed (partial denervation, PD).<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>After PD, the amplitude of excitatory junction potentials was halved but the amplitudes of contractions of isolated segments of PD arteries were of normal amplitude.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          The effects of \u03b1\n                          <jats:sub>2<\/jats:sub>\n                          \u2010adrenoceptor mediated auto\u2010inhibition of noradrenaline release and prejunctional re\u2010uptake of released noradrenaline were not reduced after PD.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          The normal contraction amplitude could not be explained by upregulation of junctional or extra\u2010junctional adrenoceptors after PD, although slightly increased \u03b1\n                          <jats:sub>2<\/jats:sub>\n                          \u2010adrenoceptor sensitivity prolonged contraction duration, amplifying responses during continuous stimulation.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>A surprising conclusion is that post\u2010receptor mechanisms activated by noradrenaline released from sympathetic nerves are normally saturated. If this applies to other arteries, it significantly changes understanding of their control by sympathetic nerves.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Abstract\u2002<\/jats:bold>\n                    Following reinnervation of denervated rat tail arteries, nerve\u2010evoked contractions are at least as large as those evoked in normally innervated arteries despite a much lower nerve terminal density. Here nerve\u2010evoked contractions have been investigated after transection of half the sympathetic innervation of normal tail arteries. After 1 week, the noradrenergic plexus 50\u201370 mm along the tail was about half as dense as control. Excitatory junction potentials recorded in smooth muscle cells of arterial segments isolated\n                    <jats:italic>in vitro<\/jats:italic>\n                    were half their normal amplitude. Surprisingly, nerve\u2010evoked contractions of isometrically mounted segments were not reduced in amplitude, as was also the case after only 3 days. After 1 week, enhancement of nerve\u2010evoked contractions by blocking either neuronal re\u2010uptake of noradrenaline with desmethylimipramine or prejunctional \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptors with idazoxan was similar to control, suggesting that these mechanisms are matched to the number of innervating axons. The relative contribution of postjunctional \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptors to contractions evoked by long trains of stimuli was enhanced but that of \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    \u2010adrenoceptors was unchanged. Transiently, sensitivity to the \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    \u2010adrenoceptor agonist phenylephrine was slightly increased. After 7 weeks, amplitudes of nerve\u2010evoked contractions remained similar to control, and sensitivity to phenylephrine had recovered but that to the \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptor agonist clonidine was slightly raised. The normal amplitude of nerve\u2010evoked contractions after partial denervation is only partly explained by the greater contribution of \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptors. While the post\u2010receptor mechanisms activated by nerve\u2010released transmitter may be modified to amplify the contractions after partial denervation, our findings suggest that these mechanisms are normally saturated, at least in this artery.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2012.250365","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T02:37:47Z","timestamp":1365043067000},"page":"2867-2884","source":"Crossref","is-referenced-by-count":6,"title":["Removal of half the sympathetic innervation does not reduce vasoconstrictor responses in rat tail artery"],"prefix":"10.1113","volume":"591","author":[{"given":"Diana","family":"Tripovic","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elspeth M.","family":"McLachlan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James 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