Effects of clonidine, dihydralazine and splanchnic nerve stimulation on the release of neuropeptide Y, MET-enkephalin and catecholamines from dog adrenal medulla

Abstract

Various neuropeptides are costored together with catecholamines in the adrenal medulla. The concurrent release (evaluated by adrenal vein plasma levels) of these neuropeptides [neuropeptide Y (NPY), met-enkephaline (ME)] and catecholamines [adrenaline (A) and noradrenaline (NA)] from the adrenal gland was examined in chloralose-anesthetized dogs after intravenous administration of clonidine (10 micrograms/kg) and dihydralazine (1 mg/kg). These results were compared to those obtained after the stimulation of the right splanchnic nerve at 1, 5 and 10 Hz frequencies. The increment in the release of catecholamines and neuropeptides was evaluated for dihydralazine and splanchnic nerve stimulation. Dihydralazine (at its maximal effect) induced a significant preferential increase in catecholamines (expressed as mean (SEM): NA: 17.3 (5.4) fold, A: 13.1 (2.6) fold) and ME (16.0 (7.1) fold) versus basal values. However, the significant increase in NPY-LI was only 2.0 (0.4) times the baseline. Splanchnic nerve stimulation induced a frequency-dependent increase in catecholamines and neuropeptides. When the stimulation frequency was increased from 1 Hz to 5 Hz, NA and A levels increased 17.9 (4.3) and 14.0 (2.2) fold, respectively and ME levels 14.1 (3.0) fold. By contrast, NPY-LI was increased only 2.3 (0.3) fold under the same conditions. Increasing the stimulation frequency from 5 Hz to 10 Hz resulted in similar elevations of NA, ME, and NPY-LI adrenal plasma levels (about 4 times) whereas A only increased twice. Clonidine decreased catecholamine and ME adrenal plasma levels (the maximal percent decrease when compared with control values was about 75%) whereas NPY adrenal plasma levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Gap junction signalling is a stress-regulated component of adrenal neuroendocrine stimulus-secretion coupling in vivo

“…In response to electrical splanchnic nerve stimulation (0.1 and 4 Hz), adrenal catecholamine output significantly increased with stimulation frequency. In particular, HF stimulation vigorously enhanced the release of both E and NE, as reported in other species 15,23,24,30,34 . E and NE can be differentially released from the adrenal, depending on splanchnic nerve stimulation frequency.…”

“…In addition, the specie, collection technique and stimulation protocols varied from one study to the other, thus precluding trivial quantitative comparison. Basal and splanchnic nerve stimulation-evoked release of adrenal catecholamines has been directly measured in adrenal-venous blood only in a few cases, in the cat 30,31 , rat 15,23,32,33 and dog 34,35 but not in the mouse. Our in vivo data indicate a basal E:NE ratio close to 10:1 in the mouse.…”

Distinct fusion properties of synaptotagmin-1 and synaptotagmin-7 bearing dense core granules

“…Basal secretion is linked with the cavicapture fusion mode, in which granules fuse and release contents through a transient opening, which reseals (Taraska et al ., 2003; Perrais et al ., 2004). Acute stress dramatically up-regulates not only the level of catecholamines in the circulation, but also a variety of neuropeptides with roles in the peripheral response (Damase-Michel et al ., 1993; Edwards and Jones, 1993; de Diego et al ., 2008). The increased sympathetic activation of the adrenal medulla during stress is linked with full-collapse fusion.…”

Spatial and activity-dependent catecholamine release in rat adrenal medulla under native neuronal stimulation

“…It has been demonstrated that with splanchnic nerve stimulation, there is a frequency‐dependent shift in catecholamine release, in which norepinephrine and epinephrine release exhibit specific frequency dependence (Damase‐Michel et al. ). Thus, there must be a differential stimulation mechanism for norepinephrine‐ versus epinephrine‐secreting cells.…”

“…Early studies of the sympathoadrenal stress response demonstrated a stressor-dependent preferential release of epinephrine or norepinephrine from the adrenal medulla to initiate the appropriate physiological response to the given stressor (Coupland 1958;Klevans and Gebber 1970;Vollmer et al 1992;Vollmer 1996;Goldstein 2010;Kvetnansky et al 2013). It has been demonstrated that with splanchnic nerve stimulation, there is a frequency-dependent shift in catecholamine release, in which norepinephrine and epinephrine release exhibit specific frequency dependence (Damase-Michel et al 1993). Thus, there must be a differential stimulation mechanism for norepinephrine-versus epinephrine-secreting cells.…”