Involvement of arginine vasopressin in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats

Jochem, Jerzy

doi:10.1007/s00011-004-1251-7

Cited by 31 publications

(51 citation statements)

References 43 publications

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“…Indeed, we previously showed in dogs that activation of mast cells located in the ME stimulates the HPA axis via histamine released within the CNS, either in response to an antigenic challenge following passive sensitization by IgE (41) or in response to C48/80 given into the V III (42). Here, in a study designed to examine whether brain mast cells might be the source of the central histamine that is known to participate in the regulation of both renin (5,30,33,44,55) and ADH (2, 7, 15, 57) secretion, we first showed that an intracerebroventricular administration of C48/80 evokes a marked increase in renin secretion and significant increases in plasma ADH and Epi.…”

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

“…In the view of the increases in renin and ADH secretions evoked by central mast cells, previous studies have shown that the concentration of histamine in the brain increases during hemorrhage (30) or dehydration (33) and that central histamine participates in hemorrhage-induced renin secretion (29,30,44). Furthermore, manipulations that increase the central histamine content [e.g., an administration either of histamine itself (29) or of a histamine N-methyl transferase inhibitor (30) into the V III ] rescue animals from critical hemorrhagic hypotension by increasing MAP and HR via an activation of the reninangiotensin system (30) and may be via release of ADH, too. There is growing recognition that activation of the HPA axis by brain mast cells may contribute to the suppression of the immediate hypersensitivity reactions and subsequent inflammation induced by peripheral mast cells (23,41) since glucocorticoids can reduce the severity of the cardiovascular dysfunction (34,47,50) and suppress the immune response (11,47,50).…”

Section: Discussionmentioning

confidence: 99%

“…Each venous blood sample (about 3 ml) was delivered into a chilled tube containing heparin at a rate of 2 ml/min. Sampling was done at nine time points: 10 min before, and 5,10,20,30,40,60,90, and 120 min after the start of an intracerebroventricular infusion of either C48/80 (Sigma-Aldrich) or histamine (Sigma-Aldrich). Value of measures (PRA and ADH) at 0 min in figures were substituted by that at 10 min before the start of intracerebroventricular infusion of the corresponding each experiment.…”

Section: Methodsmentioning

confidence: 99%

“…Antidiuretic hormone (ADH), along with the renin-angiotensin system, is of great importance in regulating the defenses against both stress and cardiovascular dysfunction (57). The stress-induced increases in both renin secretion (5,14,29,30,33,44,55) and ADH (2,7,15,57) depend upon increases in the production of histamine and its receptors. Thus, these data seem to suggest that in the regulation of both renin and ADH secretion during stress reactions, histamine may act as a neurotransmitter within the hypothalamus (14,25,33,54,59).…”

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confidence: 99%

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Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Matsumoto¹,

Inoue²,

Shimada³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Because degranulation of brain mast cells activates adrenocortical secretion ( 41 , 42 ), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 μg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na+, K+, and Cl−), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H1histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H2histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 μg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Matsumoto¹,

Inoue²,

Shimada³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Cardiovascular effects of the microinjection of L‐proline into the third ventricle or the paraventricular nucleus of the hypothalamus in unanesthetized rats

Lopes-Azevedo

Scopinho

Busnardo

et al. 2012

J of Neuroscience Research

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We investigated the cardiovascular effects of the microinjection of L-proline (L-Pro) into the third ventricle (3V) and its peripheral mechanisms. Different doses of L-Pro into the 3V caused dose-related pressor and bradycardiac responses. The pressor response to L-Pro injected into the 3V was potentiated by intravenous pretreatment with the ganglion blocker pentolinium (5 mg/kg), thus excluding any significant involvement of the sympathetic nervous system. Because the response to the microinjection of L-Pro into the 3V was blocked by intravenous pretreatment with the V1-vasopressin receptor antagonist dTyr(CH(2) )(5) (Me)AVP (50μg/kg), it is suggested that these cardiovascular responses are mediated by a vasopressin release. The pressor response to the microinjection of L-Pro into the 3V was found to be mediated by circulating vasopressin, so, given that the paraventricular nucleus of the hypothalamus (PVN) is readily accessible from the 3V, we investigated whether the PVN could be a site of action for the L-Pro microinjected in the 3V. The microinjection of L-Pro (0.033 μmoles/0.1 μl) into the PVN caused cardiovascular responses similar to those of injection of the 3V and were also shown to be mediated by vasopressin release. In conclusion, these results show that the microinjection of L-Pro into the 3V causes pressor and bradycardiac responses that could involve stimulation of the magnocellular cells of the PVN and release of vasopressin into the systemic circulation. Also, because the microinjection of L-Pro into the PVN caused a pressor response, this is the first evidence of cardiovascular effects caused by its injection in a supramedullary structure.

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Melanocortins and the Cholinergic Anti-Inflammatory Pathway

Giuliani

Ottani

Altavilla

et al. 2010

Advances in Experimental Medicine and Biology

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Experimental evidence indicates that small concentrations of inflammatory molecules produced by damaged tissues activate afferent signals through ascending vagus nerve fibers, that act as the sensory arm of an "inflammatory reflex". The subsequent activation of vagal efferent fibers, which represent the motor arm of the inflammatory reflex, rapidly leads to acetylcholine release in organs of the reticuloendothelial system. Acetylcholine interacts with α7 subunit-containing nicotinic receptors in tissue macrophages and other immune cells and rapidly inhibits the synthesis/release of tumor necrosis factor-α and other inflammatory cytokines. This neural anti-inflammatory response called "cholinergic anti-inflammatory pathway" is fast and integrated through the central nervous system. Preclinical studies are in progress, with the aim to develop therapeutic agents able to activate the cholinergic anti-inflammatory pathway. Melanocortin peptides bearing the adrenocorticotropin/α-melanocyte-stimulating hormone sequences exert a protective and life-saving effect in animals and humans in conditions of circulatory shock. These neuropeptides are likewise protective in other severe hypoxic conditions, such as prolonged respiratory arrest, myocardial ischemia, renal ischemia and ischemic stroke, as well as in experimental heart transplantation. Moreover, experimental evidence indicates that melanocortins reverse circulatory shock, prevent myocardial ischemia/reperfusion damage and exert neuroprotection against ischemic stroke through activation of the cholinergic anti-inflammatory pathway. This action occurs via stimulation of brain melanocortin MC3/MC4 receptors. Investigations that determine the molecular mechanisms of the cholinergic anti-inflammatory pathway activation could help design of superselective activators of this pathway.

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Involvement of arginine vasopressin in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats

Abstract: AVP, acting via V(1a) receptors, is involved in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats.

Cited by 31 publications

References 43 publications

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Cardiovascular effects of the microinjection of L‐proline into the third ventricle or the paraventricular nucleus of the hypothalamus in unanesthetized rats

Melanocortins and the Cholinergic Anti-Inflammatory Pathway

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