. Effect of electroacupuncture on pressor reflex during gastric distension. Am J Physiol Regul Integr Comp Physiol 283: R1335-R1345, 2002. First published August 29, 2002 10.1152/ajpregu.00192.2002The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and ␣-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 Ϯ 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1-2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5-6) over the median nerve for 30 min significantly decreased the pressor response from 33 Ϯ 6 to 18 Ϯ 4 mmHg (n ϭ 7, P Ͻ 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36-37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped (n ϭ 6, P Ͻ 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37-39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously (n ϭ 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA (n ϭ 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.

. Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats. J Appl Physiol 98: 2056 -2063, 2005. First published January 13, 2005; doi:10.1152/japplphysiol.01282.2004 at Neiguan-Jianshi acupoints through an opioid mechanism inhibits the cardiovascular pressor response induced by mechanical stimulation of the stomach. Because nociceptin also may regulate cardiovascular activity through its action in the brain stem, we hypothesized that this neuromodulator serves a role in the EA-related inhibitory effect. Blood pressure in ventilated male Sprague-Dawley rats (400 -600 g) anesthetized by ketamine and ␣-chloralose was measured during balloon inflation of the stomach. Gastric distension with 6 -8 ml of air induced consistent pressor reflexes of 26 Ϯ 1 mmHg that could be repeated every 10 min for 100 min. When nociceptin (10 nM) was microinjected into the rostral ventrolateral medulla (rVLM), the pressor response induced by gastric distension was inhibited by 68 Ϯ 6%. Thirty minutes of EA also decreased the reflex response by 75 Ϯ 11%; microinjection of saline into the rVLM did not alter the inhibitory effect of EA. In contrast, microinjection of a nociceptin receptor antagonist into the rVLM promptly reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not influence the EA-like inhibitory effect of nociceptin on the distension-induced pressor reflex (22 Ϯ 1 to 8 Ϯ 2 mmHg). Furthermore, a -opioid receptor agonist microinjected into the rVLM after microinjection of a nociceptin receptor antagonist during EA promptly reversed the nociceptin receptor antagonist-related inhibition of the EA effect. Thus, in addition to the classical opioid system, nociceptin, through opioid receptor-like-1 receptor stimulation in the rVLM, participates in the modulatory influence of EA on reflexinduced increases in blood pressure. opioids; gastric distension; somatic afferent RECENTLY, A NOVEL OPIATE-LIKE heptadecapeptide was identified in rat brain extracts (41,46). The peptide, called nociceptin (41) or Orphanin FQ (46), has a high amino acid sequence homology to classical endogenous opioid peptides (i.e., endorphins, enkephalins, endomorphins, and dynorphins) and especially to dynorphin A. Furthermore, amino acid sequencing of the receptor believed to be specific for nociceptin, or opioid receptor-like-1 (ORL-1), was found to be 47-50% identical to that of the coding sequences of -, ␦-, and -opioid receptors (10,

In children with type 1 diabetes (T1DM), altered adaptive responses to exercise (secretion of growth factors, inflammatory cytokines, and glucoregulatory mediators) may have potential implications in growth and development, early onset of disease complications, and incidence of hypoglycemia. We therefore measured a broad spectrum of exercise responses in 12 children with T1DM (seven males and five females) and 12 controls (six males / six females) aged 11-15 yr, during a 30-min exercise challenge @ 80% VO(2)max. Euglycemia was strictly controlled during exercise, and in diabetic patients a basal rate of i.v. insulin was allowed to maintain baseline insulin concentrations. Throughout the experiment, interleukin-6 (IL-6) concentrations (pg/mL) were markedly higher in T1DM vs. controls (preexercise: 5.0+/-1.3 vs. 1.9+/-0.6, p<0.02; end-exercise 5.3+/-1.2 vs. 2.7+/-1.0, p<0.05; 30-min postexercise: 8.2+/-2.2 vs. 3.9+/-0.8, p<0.05). A similar pattern was also observed with norepinephrine. Growth hormone (GH) concentration was similar in both groups at baseline and end-exercise, but in T1DM the exercise-induced GH remained significantly elevated 30 min after exercise (9.2+/-2.2 vs. 3.1+/-0.9 ng/L, p<0.01). The exercise-induced increase in glucagon elicited by exercise in controls was similar to that previously observed in healthy adults (10+/-3 pg/mL); however, it was significantly blunted in T1DM children (2+/-2 pg/mL, p<0.05). In conclusion, T1DM children displayed significant alterations in multiple aspects of their adaptive response to intense exercise.