Sodium-Induced Elevation of Blood Pressure in the Anephric State

Hatzinikolaou, Peter; Gavras, Haralambos; Brunner, Hans R.; Gavras, Irène

doi:10.1126/science.7403861

Cited by 39 publications

(21 citation statements)

References 13 publications

(6 reference statements)

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“…Subtotal nephrectomy per se was accompanied by a small tendency to elevated plasma AVP levels, as shown in figure 2, which is also in accordance with observations by other investigators 6 and probably reflects decreased elimination of AVP through the kidneys. 12 Maintenance on water ad libitum for 24 hours did not change AVP levels, whereas infusion of normal saline increased them by over fourfold.…”

Section: Discussionsupporting

confidence: 91%

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Vasopressin in salt-induced hypertension of experimental renal insufficiency.

DiPette

Gavras²,

North³

et al. 1982

Hypertension

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SUMMARY The purpose of these experiments was to determine if arginine vasopressin (AVP) contributes to the blood pressure elevation induced by salt excess in renal insufficiency. Conscious rats were studied 6 days after surgical removal of 85% renal mass, which resulted hi renal Insufficiency as evidenced by an elevation in BUN and creatlnine. Four groups of subtotally nephrectomized animals were studied; two at time zero and two following a 24-hour 0.9% NaCI Intravenous (l.v.) infusion. One group at each time had plasma AVP determined, while the other was given 30 ^g I.T. of a specific Inhibitor of the pressor effect of AVP. A fifth subtotally nephrectomized and a sixth normal nonsurgical group were observed without infusion for 24 hours, at which time plasma AVP was determined. Subtotal nephrectomy alone increased baseline BP and tended to increase plasma AVP levels over those of normal control animals. Twenty-four hour saline infusion increased BP in both infused groups by 29 ± 4 and 30 ± 3 mm Hg respectively. No change in BP occurred in either the subtotally nephrectomized or normal animals observed without infusion for 24 hours. Following saline infusion, BP decreased by 20.2 ± 1.5 in response to the AVP inhibitor as compared to 13 ± 1.5 mm Hg at time zero (p < 0.001). AVP was 42 ± 9.6 following saline infusion as compared to 10.5 ± 1.5 pg/ml at time zero (p < 0.001). Six of the saline-infused animals had urine collected over the 24 hours. The percent of Na excreted/Na infused was 83%, while the percent of volume excreted/volume infused was 91.5% (p < 0.05), demonstrating to an extent selective retention of Na as opposed to volume. Taken

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Section: Discussionsupporting

confidence: 91%

“…6 It also caused a decrease in HR, probably due to baroreceptor reflex activity. Maintenance on water ad libitum for 24 hours, without saline infusion, caused no blood pressure change from baselines in either subtotally-nephrectomized or intact animals.…”

Section: Discussionmentioning

confidence: 97%

Vasopressin in salt-induced hypertension of experimental renal insufficiency.

DiPette

Gavras²,

North³

et al. 1982

Hypertension

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“…3 ' ' 7 However, as in the present study, investigators found no immediate rise in pressure; rather, they observed an increase of blood pressure after 1 week but not earlier.…”

Section: Discussionsupporting

confidence: 50%

“…In 1980, Hatzinikolaou et al, 7 found higher blood pressures in normotensive anephric rats receiving acute infusions of hypertonic saline than in those receiving hypertonic mannitol. The pressor action of hypertonic saline was not completely inhibited by a vasopressin antagonist, and the difference between the blood pressure after vasopressin (AVP) blockade, and control was greater in the saline group.…”

mentioning

confidence: 99%

Comparable effect of isotonic infusions on blood pressure in the anephric rat.

Kleinert¹,

Leslie²,

Jh³

et al. 1983

Hypertension

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SUMMARYWhether and to what extent sodium chloride infusions elevate blood pressure acutely were examined in conscious, normotensive, and spontaneously hypertensive (SHR) anephric rats. All animals were bilaterally nephrectomized 18 hours before study.Normotensive Wistar rats, allowed no food or water post nephrectomy (Groups I-IV), received either no infusion (Group I, control) or intravenous infusion of isotonic solutions of either NaCI, mannitol, or dextrose at a rate of 0.018 ml/min for 2 hours. Mean arterial pressure (MAP) measurements were determined directly by arterial catheter for control (C), 1 hour, and 2 hours. Blood pressure was increased above control in all groups at 1 hour and 2 hours (p < 0.05). The increase in MAP with NaCI was similar to that with no infusion or infusion of mannitol or dextrose. Normotensive Wistar rats (Groups V-VI) and SHR (Group VII) were allowed free access to food and water post nephrectomy and received either no infusion (Group V, control) or infusion of isotonic saline at a rate of 0.037 ml/min for 2 hours. MAP was elevated above control in all groups (V-VII) at 1 and 2 hours (p < 0.05). The magnitude of the rise was similar among all groups. Food and water accessibility post nephrectomy did not alter results. In both sets of experiments when saline was infused we were unable to identify any increase in blood pressure greater than control at either infusion rate. In fact, we continued the saline infusion in Group VI, until 100 ml of saline was infused without any elevation in blood pressure above control. We conclude that during the 2 hours of observations neither sodium nor chloride ions exert an independent eifect on MAP in normotensive or hypertensive anephric rats when compared to no infusion or isotonic isovolemic infusions of mannitol or dextrose during the same time period. (Hypertension 5: 421-426, 1983) KEY WORDS • sodium chloride • mannitol • dextrose • Wistar Kyoto rats spontaneously hypertensive rats • acute infusions C HRONIC dietary administration of sodium chloride may elevate blood pressure under a variety of specific conditions.'" 3 It has been assumed that this action is mediated indirectly because of accompanying fluid retention and the resultant increase in intravascular volume. 4 Although the volume theory is widely accepted, other mechanisms such as release of a slow pressor substance have been suggested 5 '6 as an alternate means by which sodium chloride indirectly induces an elevation in blood pressure.Although there exists a large body of literature on chronic sodium administration and blood pressure, Received April 14, 1982; revision accepted December 8, 1982. there are few studies dealing with the effects of acute sodium administration on blood pressure. In 1980, Hatzinikolaou et al., 7 found higher blood pressures in normotensive anephric rats receiving acute infusions of hypertonic saline than in those receiving hypertonic mannitol. The pressor action of hypertonic saline was not completely inhibited by a vasopressin antagonist, and the...

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“…An increase in plasma osmolality induces several responses including an increase in sympathetic activity, blood pressure elevation, and the release of neurohormones, such as vasopressin and angiotensin II (Bealer 2000;Hatzinikolaou et al 1980Hatzinikolaou et al , 1981Stocker and Toney 2005;Weiss et al 1996). Part of these responses are mediated through activation of the hypothalamic paraventricular nucleus (PVN) driven by the circumventricular organs in which central osmoreceptors are located (Antunes-Rodrigues et al 2004;Stocker et al 2008).…”

mentioning

confidence: 99%

ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptor-mediated currents

Ferreira‐Neto

Antunes

Stern

2015

Journal of Neurophysiology

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Ferreira-Neto HC, Antunes VR, Stern JE. ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptormediated currents. J Neurophysiol 114: 159 -169, 2015. First published April 22, 2015 doi:10.1152/jn.01011.2014.-We have previously shown that ATP within the paraventricular nucleus (PVN) induces an increase in sympathetic activity, an effect attenuated by the antagonism of P2 and/or glutamatergic receptors. Here, we evaluated precise cellular mechanisms underlying the ATP-glutamate interaction in the PVN and assessed whether this receptor coupling contributed to osmotically driven sympathetic PVN neuronal activity. Whole-cell patch-clamp recordings obtained from PVN-rostral ventrolateral medulla neurons showed that ATP (100 M, 1 min, bath applied) induced an increase in firing rate (89%), an effect blocked by kynurenic acid (1 mM) or 4-[[4-Formyl-5-hydroxy-6-methyl-3-[(phosphonooxy)methyl]-2-pyridinyl]azo]-1,3-benzenedisulfonic acid tetrasodium salt (PPADS) (10 M). Whereas ATP did not affect glutamate synaptic function, ␣-amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) receptor-mediated currents evoked by focal application of AMPA (50 M, n ϭ 13) were increased in magnitude by ATP (AMPA amplitude: 33%, AMPA area: 52%). ATP potentiation of AMPA currents was blocked by PPADS (n ϭ 12) and by chelation of intracellular Ca 2ϩ (BAPTA, n ϭ 10). Finally, a hyperosmotic stimulus (mannitol 1%, ϩ55 mosM, n ϭ 8) potentiated evoked AMPA currents (53%), an effect blocked by PPADS (n ϭ 6). Taken together, our data support a functional stimulatory coupling between P2 and AMPA receptors (likely of extrasynaptic location) in PVN sympathetic neurons, which is engaged in response to an acute hyperosmotic stimulus, which might contribute in turn to osmotically driven sympathoexcitatory responses by the PVN.ATP; ␣-amino-3-hydroxy-5-methylisoxazole propionic acid; paraventricular nucleus; rostral ventrolateral medulla; hyperosmolarity BODY FLUID HOMEOSTASIS is tightly regulated by the integration of renal, cardiovascular, and neuroendocrine systems (Share and Claybaugh 1972). An increase in plasma osmolality induces several responses including an increase in sympathetic activity, blood pressure elevation, and the release of neurohormones, such as vasopressin and angiotensin II (Bealer 2000;Hatzinikolaou et al. 1980Hatzinikolaou et al. , 1981Stocker and Toney 2005;Weiss et al. 1996). Part of these responses are mediated through activation of the hypothalamic paraventricular nucleus (PVN) driven by the circumventricular organs in which central osmoreceptors are located (Antunes-Rodrigues et al. 2004;Stocker et al. 2008). The PVN is composed of magnocellular and parvocellular neurons. Magnocellular neurons synthesize and release vasopressin and oxytocin systemically from the posterior pituitary, whereas parvocellular neurons project to premotor sympathoexcitatory neurons located either in the rostral ventrolateral medulla (RVLM) and/or intermediolateral cell column of the spinal cord.Several neurotransmitters in t...

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Sodium-Induced Elevation of Blood Pressure in the Anephric State

Cited by 39 publications

References 13 publications

Vasopressin in salt-induced hypertension of experimental renal insufficiency.

Vasopressin in salt-induced hypertension of experimental renal insufficiency.

Comparable effect of isotonic infusions on blood pressure in the anephric rat.

ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptor-mediated currents

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