Central and Systemic Effects of a Vasopressin V1 Antagonist on MAP Recovery After Haemorrhage in Rats

Johnson, Janel V.; Bennett, Gerald; Hatton, R.

doi:10.1097/00005344-198810000-00005

Cited by 13 publications

(11 citation statements)

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“…It is generally accepted that AVP plays an important role in raising blood pressure upon recovery from hemorrhage-induced hypotension via V1a receptors. It has been reported that V1aR antagonist significantly delays blood pressure recovery from hemorrhage (11,19,26). Our present findings further support the physiological role of AVP in the blood pressure recovery from hemorrhage-induced hypotension.…”

Section: Discussionsupporting

confidence: 90%

“…This hormone exerts potent vasoconstrictor action through V1a receptors (V1aR) in vascular smooth muscles (23,27). It has been reported that a marked increase in plasma AVP following hemorrhage helps the recovery of blood pressure from hemorrhageinduced hypotension (11,19,26). Considerable evidence suggests the primary pathogenic role of AVP in some models of hypertension, such as the deoxycorticosterone (DOCA)-salt model (2,8,9,21).…”

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confidence: 99%

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Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Tachikawa¹,

Yokoi²,

Nagasaki³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Although arginine vasopressin (AVP), an antidiuretic hormone, has been widely acknowledged to play an important role in cardiovascular regulation via V1a receptors (V1aR), its precise significance remains unclear. In this study, we investigated the effects of long-standing high plasma AVP status on cardiovascular regulation in the AVP-overexpressing transgenic (Tg) rat. Adult male homozygous Tg rats were compared with age-matched normal Sprague-Dawley rats as controls. There were no significant differences in mean arterial blood pressure (BP; MABP) or heart rate between Tg and control rats in the basal state. Subcutaneous injection of AVP significantly increased MABP in controls but did not cause any apparent increase in MABP in Tg rats. BP recovery from hemorrhage-induced hypotension was significantly delayed in Tg compared with control rats. Pretreatment with a selective V1aR antagonist, OPC-21268, which is thought to restore the downregulation of V1aR, markedly improved both of these impaired responses. Northern blot analysis confirmed that decreased expression of V1aR mRNA and pretreatment with V1aR antagonist significantly restored the downregulation of V1aR mRNA. These results suggest that the Tg rat has decreased sensitivity to the hypertensive effect of AVP due to downregulation of V1aR, which may function as an adaptive mechanism to maintain normal BP against chronic hypervasopressinemia. In addition, impaired restoration of BP after hemorrhage-induced hypotension in Tg rats supports a physiological role of AVP in cardiovascular regulation.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Tachikawa¹,

Yokoi²,

Nagasaki³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…Rats with an indwelling LVC gave somewhat and MAP values before AVP infusion were not different attenuated HR responses compared with rats without among the four groups. As reported by others (21,30), cannulae, although the differences were not significant antagonist effects were long-lasting, since the MAP by ANOVA-RM. In general, control bradycardias were measured before testing the effects of drugs because of the unknown latencies of the drug effects in the CSF.…”

Section: Resultssupporting

confidence: 69%

“…after hemorrhage (19). In conscious Wistar rats, AVP levels rose from 5 to 108 pg/ml after 45 min (21). It is interesting that in the rabbit, major increases in AVP do not occur until 35% or more of the blood volume is lost (16), yet in the dog (20) and rat (19, 2 1,22), major increases occur after only 20-25% of blood volume is removed.…”

Section: Discussionmentioning

confidence: 98%

“…It is interesting that in the rabbit, major increases in AVP do not occur until 35% or more of the blood volume is lost (16), yet in the dog (20) and rat (19, 2 1,22), major increases occur after only 20-25% of blood volume is removed. A second reason for implicating AVP in HIB is that AVP infusion in nonhemorrhaged animals causes a marked bradycardia (10,21), even in the presence of total autonomic blockade (20). A third reason for suggesting a role for AVP in HIB is that in one study with Brattleboro rats, no bradycardia or decreased RSNA was observed during hemorrhage unless the animals were administered AVP (5).…”

Section: Discussionmentioning

confidence: 99%

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Effect of Alcohol, Neurohypophysectomy, and Vasopressin Antagonists on Hemorrhage-Induced Bradycardia in the Rat

Miller

Grattan

Averill

1993

Experimental Biology and Medicine

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During initial stages of hemorrhage in the rat, cardiovascular compensation leads to a tachycardia (mean +/- SE, 5.2 +/- 0.7%; n = 23) that helps prevent a large fall in blood pressure. This compensatory phase is followed by a decompensatory phase in which mean arterial pressure and heart rate fall. A rise in arginine vasopressin (AVP) levels has been postulated as the cause of this hemorrhage-induced bradycardia (HIB). The object of the present study was to determine whether interference with AVP release by alcohol anesthesia or neurohypophysectomy or by blockade of AVP receptors in the plasma or cerebral spinal fluid could attenuate HIB. Male Wistar rats were anesthetized with pentobarbital, surgically prepared, and bled to maintain a blood pressure of 40-50 mm Hg. After hemorrhage, heart rate decreased 15 +/- 2% (n = 6) with alcohol anesthesia compared with 32 +/- 3% (n = 7) with pentobarbital. After neurohypophysectomy, however, HIB remained unchanged (-15 +/- 2%; n = 5) compared with sham-operated controls (-19 +/- 3%; n = 6). Peripheral administration of two nonselective V1/V2 antagonists and one V2 antagonist had no effect on HIB, whereas a V1 antagonist significantly attenuated the heart rate decrease (-15 +/- 4%; n = 6) compared with controls (-32 +/- 3%; n = 7). None of the AVP antagonists tested at one tenth the peripheral dose had any effect on HIB when administered into the lateral ventricle of the brain, although a mixed serotonin, dopamine, and catecholamine antagonist, spiperone, potentiated the response. It was concluded that although peripheral release of AVP may be partially involved in the heart rate response to hemorrhage, central AVP release and central AVP receptors were not involved in HIB.

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Cardiovascular and catecholamine responses to acute haemorrhage in anaesthetized potassium-adapted rats

Obika

1993

Res. Exp. Med.

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The experiments were designed to determine whether potassium-loaded rats have a deficient recovery of blood pressure after a rapid arterial haemorrhage. Potassium loading was achieved by providing a 0.75% KCl solution as drinking fluid for 14 days, while control rats had either distilled water or tapwater. MAP, HR, Hct, and plasma electrolytes were determined before and after 1 and 2% body weight haemorrhage in anaesthetized Sprague-Dawley rats. Potassium-loaded rats had significantly reduced blood pressure recovery within 20 min after haemorrhage. HR was significantly reduced within 5 min only after 2% haemorrhage in potassium-adapted rats. Haemorrhage induced significant hyperkalaemia which was greater and significantly prolonged after 2% haemorrhage. The significant fall in Hct after haemorrhage was not affected by the magnitude of haemorrhage. In an additional group of rats, the pressor response to intravenous infusion of vasopressin was unaffected by potassium loading, whereas that to noradrenaline and angiotensin II was significantly reduced throughout the 20 min of infusion. The peak increase in blood pressure after phenylephrine injection was, however, unaffected by potassium loading. Basal plasma catecholamines concentration as well as concentrations after 1% haemorrhage were unaffected by potassium loading. It is concluded that the reduced vascular response to noradrenaline and angiotensin contributed to the reduced recovery of blood pressure after haemorrhage in potassium-loaded rats. Furthermore, the result with phenylephrine suggest a mechanism that is unrelated to direct vascular effects of noradrenaline and angiotensin II.

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Central and Systemic Effects of a Vasopressin V1 Antagonist on MAP Recovery After Haemorrhage in Rats

Cited by 13 publications

References 0 publications

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Effect of Alcohol, Neurohypophysectomy, and Vasopressin Antagonists on Hemorrhage-Induced Bradycardia in the Rat

Cardiovascular and catecholamine responses to acute haemorrhage in anaesthetized potassium-adapted rats

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