Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Recruitment of magnocellular neuroendocrine cells (m.n.c.s) to a repetitive burst pattern (phasic firing) is associated with increased vasopressin secretion from neurohypophysial terminals in the intact animal. Based on invertebrate studies, bursts of action potentials can arise in two distinct ways: as an intrinsic property of the recorded cell or as an emergent property of synaptic interactions. 2. The majority of phasic m.n.c.s in the hypothalamic slice preparation display an endogenous pace-maker mechanism underlying bursting. It is voltage dependent and varies considerably in periodicity and time course as described in the accompanying paper (Andrew, 1987). 3. In contrast to this intrinsic mechanism, the present study examined if cells might be driven by periodic synaptic input. Intracellular recordings from six of thirty-two phasic m.n.c.s in the supraoptic nucleus revealed an isoperiodic oscillation of the membrane potential, where each depolarizing phase could support a burst. 4. The oscillation had a smooth trajectory and fixed period (range, 5-17 s). The oscillatory frequency was not voltage dependent, i.e. periodicity was unaffected by steady current injection through the recording electrode. 5. The frequency and amplitude of the oscillation remained unaltered by action potential firing. The isoperiodic oscillation could abate spontaneously, leaving intact the endogenous ability to fire a triggered burst driven by an underlying plateau potential. 6. Perfusion with either 10 mM-Mg2+-0.05 mM-Ca2+ or 0.5-2.0 microM-tetrodotoxin blocked both the oscillation and evoked post-synaptic potentials, indicating that the oscillation was synaptically generated. Given that both treatments could also block the intrinsic burst process and that the oscillation could spontaneously abate, the synaptic nature of the oscillation remains a tentative but reasonable conclusion. 7. In total, the evidence suggests that the isoperiodic oscillation has a synaptic origin independent of intrinsic mechanisms. It probably results from synaptic input generated within the slice but the source is not yet identified. This input could support phasic bursting in those m.n.c.s lacking a pace-maker ability and so promote the release of vasopressin in the intact animal.
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PMID:Isoperiodic bursting by magnocellular neuroendocrine cells in the rat hypothalamic slice. 365 53

The powerful local metabolic regulation adjusting coronary blood flow to myocardial oxygen consumption under normal conditions is beyond doubt. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations, but not in steady-state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists. Recruitment of such vasodilator reserve results in improved regional myocardial blood flow and attenuated regional ischemic dysfunction. beta-adrenergic coronary dilation is of minor functional importance. alpha-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, such that myocardial oxygen extraction increases to match the increased oxygen consumption. alpha-adrenergic coronary constriction remains operative in ischemic myocardium, thus precipitating or contributing to acute myocardial ischemia during sympathetic activation and exercise in experimental animals as well as in patients with stable angina. The vagal transmitter acetylcholine--upon exogenous intracoronary infusion--induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin, and angiotensin can induce myocardial ischemia upon exogenous administration. Their pathophysiological role in myocardial ischemia and reperfusion, however, remains to be established.
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PMID:Local and neurohumoral control of coronary blood flow. 839 71

Coexposure of hypothalamo-neurohypophyseal system explants to ATP and phenylephrine [PE; an alpha1-adrenergic receptor (alpha1-AR) agonist] induces an extended elevation in vasopressin and oxytocin (VP/OT) release. New evidence is presented that this extended response is mediated by recruitment of desensitization-resistant ionotropic purinergic receptor subtypes (P2X-Rs): 1) Antagonists of the P2X2/3 and P2X7-Rs truncated the sustained VP/OT release induced by ATP+PE but did not alter the transient response to ATP alone. 2) The P2X2/3 and P2X7-R antagonists did not alter either ATP or ATP+PE-induced increases in [Ca(2+)](i). 3) P2X2/3 and P2X7-R agonists failed to elevate [Ca(2+)](i), while ATP-gamma-S, an agonist for P2X2-Rs increased [Ca(2+)](i) and induced a transient increase in VP/OT release. 4) A P2Y1-R antagonist did not prevent initiation of the synergistic, sustained stimulation of VP/OT release by ATP+PE but did reduce its duration. Thus, the desensitization-resistant P2X2/3 and P2X7-R subtypes are required for the sustained, synergistic hormone response to ATP+PE, while P2X2-Rs are responsible for the initial activation of Ca(2+)-influx by ATP and ATP stimulation of VP/OT release. Immunohistochemistry, coimmunoprecipitation, and Western blot analysis confirmed the presence of P2X2 and P2X3, P2X2/3, and P2X7-R protein, respectively in SON. These findings support the hypothesis that concurrent activation of P2X2-R and alpha1-AR induces calcium-driven recruitment of P2X2/3 and 7-Rs, allowing sustained activation of a homeostatic circuit. Recruitment of these receptors may provide sustained release of VP during dehydration and may be important for preventing hemorrhagic and septic shock.
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PMID:Sustained stimulation of vasopressin and oxytocin release by ATP and phenylephrine requires recruitment of desensitization-resistant P2X purinergic receptors. 1962 89