Opiate receptor-mediated decrease in renal nerve activity during hypotensive hemorrhage in conscious rabbits.

Morita, Hironobu; Nishida, Yasuhiro; Motochigawa, Hiroyuki; Uemura, Nobuhisa; Hara, Hiroshi; Vatner, S. F.

doi:10.1161/01.res.63.1.165

Cited by 61 publications

(27 citation statements)

References 19 publications

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“…Such (32,33). Although opiate receptor blockade with naloxone has been shown to reverse hemorrhage-induced sympathoinhibition in conscious rabbits (32,33), it has not proven to be effective in treating hemorrhagic shock in humans (34).…”

Section: Discussionmentioning

confidence: 99%

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

et al. 1992

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Acute hypotension is an important complication of hemodialysis, but the underlying mechanisms remain poorly understood. Because hemorrhage-induced hypovolemia can trigger a sudden decrease in sympathetic activity resulting in bradycardia and vasodilation, we hypothesized that hemodialysis-induced hypovolemia also can trigger the same type of vasodepressor reaction, which would exacerbate the volume-dependent fall in blood pressure. We therefore measured blood pressure, vascular resistance, and sympathetic nerve activity (intraneural microelectrodes) during sessions of maintenance hemodialysis in 7 patients with and 16 patients without a history of hemodialysis-induced hypotension. During hemodialysis, blood pressure at first remained unchanged as calf resistance increased in both hypotension-resistant (from 37±4 to 49±5 U, P < 0.05) and hypotension-prone (from 42±6 to 66±12 U, P < 0.05) patients; sympathetic activity increased comparably in the subset of patients in whom it could be measured. With continued hemodialysis, calf resistance and sympathetic activity increased further in the hypotension-resistant patients, but in the hypotensionprone patients the precipitous decrease in blood pressure was accompanied by decreases in sympathetic activity, vascular resistance, and heart rate as well as symptoms of vasodepressor syncope. On an interdialysis day, both groups of patients increased vascular resistance normally during unloading ofcardiopulmonary baroreceptors with lower body negative pressure and increased heart rate normally during unloading of arterial baroreceptors with infusion of nitroprusside. These findings indicate that in a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, hemodialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope. (J. Clin.

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Section: Discussionmentioning

confidence: 99%

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

et al. 1992

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“…Since endogenous opioids augment the extent of sympathoinhibition during a hypotensive stimulus (e.g. haemorrhage [11], sudden release of endogenous opioids in the brain could contribute to baroreflex resetting and thereby produce sympathoinhibition despite hypoten sion. Vasopressin also augments baroreflex restraint of sympathoneurai outflows [12], and extremely high circulating vasopressin levels often accompany vaso depressor syncope [13].…”

Section: Introductionmentioning

confidence: 99%

Neurohumoral antecedents of vasodepressor reactions

Jacobs

Goldstein²,

Willemsen

et al. 1995

Eur J Clin Investigation

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Abstract. Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine condi tions for this dramatic syndrome are poorly under stood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently devel oped vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -4 0 mmHg 11 subjects had vasodepressor reac tions, with sudden hypotension, nausea, and dizzi ness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15mmHg (A^-0*06± (S E M ) 0*04pmol m in'1100 mL" 1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (A = 0*31 ±0* 13 pmol m in '1 lOOmL" 1). Plasma levels of /?-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40 mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinbibition, and release of endogenous opioids can precede vasode pressor syncope.

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“…The control capacity of the baroreflex AP control system progressively decreased with time after massive hemorrhage and tended to recover somewhat by 110 min after hemorrhage. Therefore, the evaluation of the baroreflex AP control capacity under the hypovolemic conditions due to massive hemorrhage, including estimation of time-dependent effects of anesthetics, is not considered to show the precise control capacity of the system because massive hemorrhage must be a parametric forcing which modifies the normal characteristics of the baroreflex AP control system [6][7][8][9][16][17][18].…”

Section: Discussionmentioning

confidence: 99%

Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

et al. 2000

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Abstract:The present study is designed to investigate the time-dependent effect of pentobarbital anesthesia on the baroreflex arterial pressure (AP) control system in rabbits. The overall AP control capacity of the baroreflex system was assessed with mean arterial pressure (MAP) responses to the rapid mild hemorrhage (2 ml/kg body weight) and an overall open-loop gain (G) of the system. The G value was determined by means of the following formula: G=∆AP I /∆AP S -1, where ∆AP I is an immediate MAP fall and ∆AP S a steady-state fall after the rapid hemorrhage. Prior to the experiment, two catheters for AP measurement and hemorrhage were chronically in-dwelt in the aortic arch via the left subclavian and left common carotid arteries, respectively. Control mean arterial pressure averaged for 30 sec before the rapid hemorrhage (CMAP), ∆AP I and ∆AP S significantly increased and reached the maximal value at 14 min (CAMP: p<0.01) and 28 min (∆AP I : p<0.01 and ∆AP S : p<0.01) after the intravenous injection of sodium pentobarbital in a 25.0 mg/kg dose, respectively. These values gradually decreased in the course of time and tended to recover to near the preanesthetic level at 77-98 min after the anesthesia. The G value significantly decreased from 7.3 in the conscious state to 1.5 at 28 min after the anesthesia (p<0.001), gradually increased with lapse of time and recovered to near the preanesthetic level at 77-98 min after the anesthesia. No significant difference in G was observed between in the conscious and anesthetized states beyond 70 min after the anesthesia (p>0.05). These findings suggest that pentobarbital sodium exerts a timedependent inhibitory effect on the baroreflex system but does not significantly affect the overall AP control capacity of the baroreflex system itself at least 70 min after the intravenous administration at a dose of 25.0 mg/kg.

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Opiate receptor-mediated decrease in renal nerve activity during hypotensive hemorrhage in conscious rabbits.

Cited by 61 publications

References 19 publications

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

Neurohumoral antecedents of vasodepressor reactions

Time-Dependent Change in Baroreflex Control Capacity of Arterial Pressure by Pentobarbital Anesthesia in Rabbits.

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