Increased Circulating Vasopressin May Account for Ethanol-induced Hypertension in Rats

Resstel, Leonardo Barbosa Moraes; Scopinho, América A.; Silva, Andreia Lopes da; Rodrigues, Josemar; Corrêa, Fernando Morgan de Aguiar

doi:10.1038/ajh.2008.189

Cited by 18 publications

(16 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After paralysis, anesthesia was monitored by the stability of AP and HR, and supplements equal to 10% of the initial dose were given when needed. End-tidal PCO2 was continuously monitored and maintained within normal limits (35)(36)(37)(38)(39)(40) by adjusting ventilation rate (80 -100 breaths/min) and/or tidal volume (2.0 -3.0 ml). Body temperature was held at 37°C with a water-circulating pad.…”

Section: Methodsmentioning

confidence: 99%

“…We conclude that ethanol and acetate increase sympathetic outflow and arterial pressure, which may involve the activation of NMDA receptors in CeA neurons projecting to the RVLM. amygdala; acetate; ethanol; glutamate receptors; sympathetic nerve activity; N-methyl-D-aspartate ALCOHOL CONSUMPTION is able to cause an increase in arterial pressure (AP) and/or sympathetic outflow in both humans (8,19,21,26,37,59) and animals (9,38,39,42,57). Increased secretion of arginine vasopressin (38) and corticotrophin-releasing hormone (37), as well as enhanced vascular reactivity to the vasoconstrictor agent phenylephrine (39, 57), may underlie the mechanisms responsible for the alcohol-induced increased in AP.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats

Chapp

Gui

Huber

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

The central nervous system plays an important role in regulating sympathetic outflow and arterial pressure in response to ethanol exposure. However, the underlying neural mechanisms have not been fully understood. In the present study, we tested the hypothesis that injection of ethanol in the central nucleus of the amygdala (CeA) increases sympathetic outflow, which may require the activation of local ionotropic excitatory amino acid receptors. In anesthetized rats, CeA injection of ethanol (0, 0.17, and 1.7 μmol) increased splanchnic sympathetic nerve activity (SSNA), lumbar sympathetic nerve activity (LSNA), and mean arterial pressure (MAP) in a dose-dependent manner. A cocktail containing ethanol (1.7 μmol) and kynurenate (KYN), an ionotropic excitatory amino acid receptor blocker, showed significantly blunted sympathoexcitatory and pressor responses compared with those elicited by CeA-injected ethanol alone (P < 0.01). A cocktail containing ethanol and d-2-amino-5-phosphonovalerate, an N-methyl-d-aspartate (NMDA) receptor antagonist, elicited attenuated sympathoexcitatory and pressor responses that were significantly less than ethanol alone (P < 0.01). In addition, CeA injection of acetate (0.20 μmol, n = 7), an ethanol metabolite, consistently elicited sympathoexcitatory and pressor responses, which were effectively blocked by d-2-amino-5-phosphonovalerate (n = 9, P < 0.05). Inhibition of neuronal activity of the rostral ventrolateral medulla (RVLM) with KYN significantly (P < 0.01) attenuated sympathoexcitatory responses elicited by CeA-injected ethanol. Double labeling of immune fluorescence showed NMDA NR1 receptor expression in CeA neurons projecting to the RVLM. We conclude that ethanol and acetate increase sympathetic outflow and arterial pressure, which may involve the activation of NMDA receptors in CeA neurons projecting to the RVLM.

show abstract

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats

Chapp

Gui

Huber

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…These results indicate that the chemoreflex, which is a sympathoexcitatory reflex, may not be involved in the increased sympathetic or decreased parasympathetic activities and consequent hypertension observed in rats after ETOH exposure (2,3). In agreement with this notion, ETOH was reported to have an inhibitory effect on chemoreflexes by Sun and Reis (20), who showed that the increased blood pressure and vasomotor neuronal activity (located in the rostroventrolateral area of the medulla oblongata) in response to intracarotid cyanide administration were markedly attenuated following acute ETOH exposure.…”

Section: Discussionmentioning

confidence: 82%

“…Evidence in the literature has shown that ethanol (ETOH) exposure stimulates changes in the neuroendocrine and autonomic nervous systems (1-3). The characterized autonomic nervous system changes include an enhanced cardiac sympathetic baroreflex and a reduced cardiac parasympathetic baroreflex (2,4).…”

Section: Introductionmentioning

confidence: 99%

“…The characterized autonomic nervous system changes include an enhanced cardiac sympathetic baroreflex and a reduced cardiac parasympathetic baroreflex (2,4). In addition, diminished baroreflex control, which is a sympathoinhibitory reflex, may be involved in increased arterial pressure (2), as observed in experimental animals and humans upon ETOH exposure (2,3),. Moreover, relationships between ETOH consumption and increased mortality have been reported (11,12).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

Sabino

Silva

Resstel

et al. 2014

Clinics

View full text Add to dashboard Cite

OBJECTIVE:The effect of chronic ethanol exposure on chemoreflexes has not been extensively studied in experimental animals. Therefore, this study tested the hypothesis that known ethanol-induced autonomic, neuroendocrine and cardiovascular changes coincide with increased chemoreflex sensitivity, as indicated by increased ventilatory responses to hypoxia and hypercapnia.METHODS:Male Wistar rats were subjected to increasing ethanol concentrations in their drinking water (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). At the end of each week of ethanol exposure, ventilatory parameters were measured under basal conditions and in response to hypoxia (evaluation of peripheral chemoreflex sensitivity) and hypercapnia (evaluation of central chemoreflex sensitivity).RESULTS:Decreased respiratory frequency was observed in rats exposed to ethanol from the first until the fourth week, whereas minute ventilation remained unchanged. Moreover, we observed an increased tidal volume in the second through the fourth week of exposure. The minute ventilation responses to hypoxia were attenuated in the first through the third week but remained unchanged during the last week. The respiratory frequency responses to hypoxia in ethanol-exposed rats were attenuated in the second through the third week but remained unchanged in the first and fourth weeks. There was no significant change in tidal volume responses to hypoxia. With regard to hypercapnic responses, no significant changes in ventilatory parameters were observed.CONCLUSIONS:Our data are consistent with the notion that chronic ethanol exposure does not increase peripheral or central chemoreflex sensitivity.

show abstract

Electrophysiological properties and augmented catecholamine release from chromaffin cells of WKY and SHR rats contributing to the hypertension development elicited by chronic EtOH consumption

Bomfim

Méndez-López

Fernández-Morales

et al. 2017

European Journal of Pharmacology

View full text Add to dashboard Cite

It is known that chronic ethanol (EtOH) consumption leads to hypertension development and has been associated with deleterious effects on the cardiovascular system. Whether this condition alters calcium (Ca) signaling and exocytosis in adrenal chromaffin cells (CCs) as the case is for genetic hypertension, is unknown. We explored this question in four randomized experimental groups, male Wistar Kyoto (WKY/EtOH) and Spontaneously Hypertensive (SHR/EtOH) rats were subjected to the intake of increasing EtOH concentrations (5-20%, for 30 days) and their respective controls (WKY/Control and SHR/Control) received water. WKY/EtOH developed hypertension and cardiac hypertrophy; blood aldehyde dehydrogenase (ALDH) and HO were also augmented. In comparison with WKY/Control, CCs from WKY/EtOH had the following features: (i) depolarization and higher frequency of spontaneous action potentials; (ii) decreased Ca currents with slower inactivation; (iii) decreased K currents; (iv) augmented K-elicited cytosolic Ca transients ([Ca]); (v) enhanced K-elicited catecholamine release. These cardiovascular, blood and CCs changes were qualitatively similar to those undergone by SHR/Control and SHR/EtOH. The results suggest that the hypertension elicited by chronic EtOH has pathogenic features common to genetic hypertension namely, augmented [Ca] transients and catecholamine release from their CCs.

show abstract

Increased Circulating Vasopressin May Account for Ethanol-induced Hypertension in Rats

Cited by 18 publications

References 21 publications

Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats

Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

Electrophysiological properties and augmented catecholamine release from chromaffin cells of WKY and SHR rats contributing to the hypertension development elicited by chronic EtOH consumption

Contact Info

Product

Resources

About