Renal responses of the cardiac-denervated nonhuman primate to blood volume expansion.

Peterson, Tim O.; Jones, C. E.

doi:10.1161/01.res.53.1.24

Cited by 16 publications

(8 citation statements)

References 36 publications

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“…Although the role of atrial volume receptors in the control of ADH secretion has been demonstrated in dogs (Gauer er al., 1970;Gauer & Henry, 1976, 1983, data from studies using the non-human primate have suggested that these receptors may play a small role in regulating blood volume. Furthermore, cervical vagotomy (Gilmore et al, 1979) or complete, selective cardiac denervation (Peterson & Jones, 1983) failed to attenuate the diuretic response to volume expansion or water immersion in the monkey, although ADH levels were not measured in these animals. 1976;Linden, 1976;Fater et al, 1982) failed to elicit any renal effects in either the anaesthetized or conscious monkey (Gilmore & Zucker, 1978b;Peterson ef al., 1980Peterson ef al., , 1983Cornish & Gilmore, 1982).…”

Section: Discussionmentioning

confidence: 99%

“…According to the Henry-Gauer hypothesis (Gauer el al., 1970;Gauer & Henry, 1983), the sudden shift in fluids from the legs and abdomen into the chest and head leads to stretch of low pressure receptors (located in the atrium and/or pulmonary circulation) as evidence of an increase in total circulating blood volume. Recently the importance of the proposed Henry-Gauer atrial receptors in control of ADH responses to acute blood volume shifts in man have been challenged by observations that vagotomized non-human primates exhibit significant diuresis during water immersion or volume expansion (Gilmore & Zucker, 1978a;Peterson & Jones, 1983). Most of the evidence supporting this hypothesis has come from studies using the dog (Gauer & Henry, 1976;Linden, 1976;Donald & Shepherd, 1978), where the receptors have been shown to be primarily located in the atrial wall and the ADH response to be abolished by vagotomy.…”

Section: Introductionmentioning

confidence: 99%

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Haemodynamic and ADH responses to central blood volume shifts in cardiac‐denervated humans

Convertino

Thompson

Benjamin

et al. 1990

Clinical Physiology

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Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Haemodynamic and ADH responses to central blood volume shifts in cardiac‐denervated humans

Convertino

Thompson

Benjamin

et al. 1990

Clinical Physiology

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“…The absence of such compensatory adjustments is also consistent with the apparent lack of functional arterial baroreceptors in this species (19). In contrast, arterial pressure changes are not observed following cardiac denervation in dogs (23,24) or in a nonhuman primate (25).…”

Section: Asotocin In Chickensmentioning

confidence: 98%

Prolongation by Warfarin of "Template" Bleeding Time in Rats: A Vitamin K-Dependent Effect

Reyers

Gaetano

Donati

1986

Experimental Biology and Medicine

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Administration of warfarin to rats induced not only the well-known anticoagulant effect, but also an impairment of primary hemostasis as reflected by a significant prolongation of the "template" bleeding time. This effect was very closely associated with lowering of the prothrombin complex level and was reversed by administration of vitamin K. It is suggested that some of the clotting factors known to be vitamin Kdependent also play a role in primary hemostasis; alternatively, a putative vascular "bleeding factor" could be modulated by vitamin K availability. 0 1986 Society for Experimental Biology and Medicine.We have previously shown that warfarin prevents thrombus formation in a vascular prosthesis model in rats (1). In the context of a larger study on the mechanism of warfarin's antithrombotic effect in rats, we observed that warfarin anticoagulation was accompanied by impairment of primary hemostasis as measured by the "template" bleeding time in the rat tail (2). This finding was somewhat unexpected, since the "template" bleeding time in rats is considered to reflect mainly the early steps of hemostatic plug formation involving blood platelets and the vascular wall function or tone (2). Indeed, in severe thrombocytopenia, some antiplatelet agents and vasodilators significantly prolonged the "template" bleeding time in rats (2). In contrast, heparin at full anticoagulant doses had no such effect (2).We report here experiments designed to provide a better understanding of the mechanisms underlying the prolongation of "template" bleeding time in warfarin-treated rats.Material and Methods. CD-COBS male rats (Charles River, Calco, Italy) weighing 250-280 g, were treated with racemic warfarin (Coumadin, Endo Laboratories, Garden City, N.Y.). The drug was dissolved in isotonic saline and intravenously injected at three different doses (0.2-0.4 or 1 mg/kg body wt) to achieve different degrees of anticoagulation. Bleeding time was measured 2 to 24 hr later by applying an automated device ("template")(3) on the rat tail (9 cm from the tip) as previously described (2,4). The anticoagulant effect of warfarin was monitored immediately after bleeding time by the Thrombotest, adapted to native peripheral blood (Immuno S.p.A., Pisa, Italy). In a subsequent experiment Vitamin K1, dissolved in 6% Tween 80, was injected im 6 hr before the bleeding time test (1 mg/kg body wt vitamin K, 18 hr after 1 mg/ kg body wt warfarin).Results and Discussion. Warfarin treatment resulted within 24 hr in different levels of anticoagulation. The animals were subdivided into four groups according to their Thrombotest levels, as indicated in Fig. 1. A fifth group of rats (treated with isotonic saline) acted as a control.The bleeding times were longer than those in the control group (P < 0.01 at Duncan new multiple range test) in the two groups with Thrombotest levels below 20%. Bleeding times longer than 500 sec were found in all rats but one with a Thrombotest level below 10% ( X = 28.5 1, P < 0.Oc)l).We then addressed the issue of whether or...

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“…For example, selective ablation of volume receptor neural pathways such as thoracic dorsal rhizotomy (10), vagotomy-sinoaortie denervation (10), thoracic sympathectomy (3) or cardiac denervation (24) does not attenuate the renal excretory responses of the anesthetized monkey to volume expansion. However, this failure of selective denervations to affect these responses could be due to these mechanisms being functionally redundant.…”

Section: Introductionmentioning

confidence: 99%

Cardiopulmonary and sinoaortic baroreceptors and volume expansion in the monkey

et al. 1986

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Experiments were performed to determine the effect of combined cardiopulmonary and and sinoaortic baroreceptor denervation on the renal responses of the anesthetized nonhuman primate to acute intravascular volume expansion. Adult male Macaca fascicularis monkeys underwent chronic bilateral thoracic sympathectomy (middle cervical ganglion--T6) or sham surgery performed in two stages. After a 1-3 week recovery period, each animal was anesthetized with sodium pentobarbital and subjected to cervical vagotomy--sinoaortic denervation or further sham denervation. Estimated blood volume was then acutely expanded 20% with 6% dextran in isotonic saline. Control renal excretory function did not differ between the two groups, and both groups had similar increases in urine flow, sodium excretion, osmolar clearance, free water clearance and renal plasma flow after volume expansion. The patterns of the responses showed some group differences in that the increases in renal excretion after volume-loading had an earlier onset in the denervated animals. These results demonstrate that combined ablation of thoracic sympathetic, vagal and sinoaortic neural pathways does not compromise the ability of the nonhuman primate to increase salt and water excretion when blood volume is acutely expanded. Therefore, these neural mechanisms are not necessary for eliciting the renal responses to this hypervolemic stimulus in this species during the anesthetized state.

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Renal responses of the cardiac-denervated nonhuman primate to blood volume expansion.

Cited by 16 publications

References 36 publications

Haemodynamic and ADH responses to central blood volume shifts in cardiac‐denervated humans

Haemodynamic and ADH responses to central blood volume shifts in cardiac‐denervated humans

Prolongation by Warfarin of "Template" Bleeding Time in Rats: A Vitamin K-Dependent Effect

Cardiopulmonary and sinoaortic baroreceptors and volume expansion in the monkey

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