Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

Behm, Robert; Mewes, H.; Keizer, W. H. DeMuinck; Unger, Travis L.; Rettig, Rainer

doi:10.1152/jappl.1993.74.6.2795

Cited by 14 publications

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“…The respiratory, cardiovascular and renal responses induced in the rat by moderate hypoxia in the present study were comparable with those we reported recently (Neylon et al 1995 (Behm, Mewes, DeMuinck Keizer, Unger & Rettig, 1993). The present study provided the additional information that moderate hypoxia was accompanied by a 2-8-fold increase in plasma renin activity as might be explained by the reflex response to peripheral chemoreceptor stimulation, baroreceptor unloading and the fall in RPP (see the introduction, and below).…”

Section: Discussionsupporting

confidence: 92%

The role of the renin‐angiotensin system in the renal response to moderate hypoxia in the rat.

Neylon

Marshall

Johns

1996

The Journal of Physiology

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1. In two groups of Saffan-anaesthetized rats, we studied the role of the renin-angiotensin system in mediating the antidiuresis and antinatriuresis induced by moderate systemic hypoxia. 2. In both groups, a first period of hypoxia (breathing 12% 02 for 20 min) induced a fall in arterial partial pressure of 02 (Pa°2; to 42 mmHg), a fall in mean arterial pressure (MABP), no change in renal blood flow (RBF) due to an increase in renal vascular conductance (RVC = RBF/MABP) and falls in urine flow and absolute sodium excretion (UNa V). Concomitantly, plasma renin activity increased from 3-08 + 0-68 (mean + S.E.M.) to 8 36 + 18 ng ml-hrF. 3. In group 1 (n = 11), Losartan (10 mg kg-, i.v.), the angiotensin (AII) AT1 receptor antagonist, induced a fall in MABP (115 + 3 to 90 + 3 mmHg), an increase in RVC such that RBF was unchanged, and falls in glomerular filtration rate (GFR), urine flow and UNa V. However, hypoxia induced qualitatively similar changes to those seen before Losartan treatment. 4. In group 2 (n = 9), we occluded the aorta distal to the renal artery to prevent basal MABP and renal perfusion pressure (RPP) from falling after addition of Losartan and to keep the hypoxia-induced fall in MABP the same as before Losartan treatment. Nevertheless, Losartan induced an increase in basal RVC, RBF, urine flow and UNa V whilst hypoxia induced falls in urine flow and UN. V that were proportionately similar to those seen prior to addition of Losartan. 5. These results indicate that in the Saffan-anaesthetized rat, AII exerts tonic, renal vasoconstrictor and consequent antidiuretic and antinatriuretic influences in normoxia, but does not contribute to the hypoxia-induced antidiuresis and antinatriuresis. We propose that renin secretion is increased by the hypoxia-induced fall in RPP rather than by an increase in renal sympathetic activity. Thus, the AII generated cannot produce antidiuresis and antinatriuresis by its known facilitatory influence on the actions of an increase in sympathetic activity on the renal tubules and is insufficient to produce these effects by direct actions. Rather, these results support the view that the antidiuresis and antinatriuresis of moderate hypoxia is predominantly due to the fall in RPP.Some individuals who climb to high altitude show diuresis and natriuresis and tolerate the hypoxia well. Others show antidiuresis and antinatriuresis and commonly succumb to mountain sickness (Milledge & Catley, 1984;Honig, 1989). The antidiuresis and antinatriuresis has been attributed to the actions of angiotensin II (AII) upon the kidney, the AII being generated by hypoxia-induced stimulation of the renin-angiotensin system (Milledge & Catley, 1984.Although an increase in renin secretion might be explained as a reflex response to an increase in renal sympathetic activity caused by hypoxic stimulation of peripheral chemoreceptors (Marshall, 1994), this conclusion cannot be firmly drawn from high altitude studies, because those who climb to high altitude not only experience systemic hypoxia, but also ...

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Section: Discussionsupporting

confidence: 92%

The role of the renin‐angiotensin system in the renal response to moderate hypoxia in the rat.

Neylon

Marshall

Johns

1996

The Journal of Physiology

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“…It is notable that the changes in Pa.O2 and Pa,co2 recorded during the present study were very similar to those reported by Behm et al (1993) in unanaesthetized rats subjected to a 30 min period of breathing 125% 02. However, the fall in ABP in the unanaesthetized rats was substantially smaller in absolute and percentage terms.…”

Section: Respiratory and Systemic Cardiovascular Changessupporting

confidence: 91%

The effects of systemic hypoxia on renal function in the anaesthetized rat.

Neylon

Marshall

Johns

1995

The Journal of Physiology

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1. In rats anaesthetized with Saffan, renal function was monitored from the left kidney from the 5th minute of spontaneous breathing of 12% 02 for two 20 min periods and during air breathing before, between and after the hypoxic periods. Two groups of animals (I and II) were used, each group comprising two subgroups in which the left kidney was innervated or denervated, respectively; in Group II, renal perfusion pressure (RPP) was maintained during the 2nd hypoxic period by occl97uding the distal aorta.2. In both subgroups of Group I, both hypoxic periods produced hyperventilation, arterial P02falling to -50 mmHg. Concomitantly, mean arterial pressure (MABP) fell by similar extents (-23 %, from a baseline level of 140 mmHg during the 2nd hypoxic period). In the innervated subgroup, renal vascular conductance (RVC) increased, but glomerular filtration rate (GFR) fell (by 48 and 6%, respectively, during the 2nd hypoxic period), while urine flow, absolute sodium excretion (UNa V) and fractional sodium excretion (FENa) fell (by 52, 63 and 61 %, respectively). Baseline urine flow, UN. V and FENa were higher in the denervated subgroup, but hypoxia produced similar percentage changes from baseline in all variables. 3. In Group II, both subgroups showed similar changes during the 1st hypoxic period as the corresponding subgroups of Group I. However, during the 2nd hypoxic period when the fall in MABP was reduced to 7%, the increase in RVC persisted only in the denervated subgroup; there was no significant change in GFR, urine flow, UNaV or FENa in either subgroup. 4. These results indicate that, in the rat, moderate hypoxia produces antidiuresis and antinatriuresis that are not dependent on the renal nerves, but are dependent on the hypoxiainduced fall in MABP. The fall in renal perfusion pressure (RPP) may directly determine renal function, but reflex influences upon the kidney initiated by, for example, arterial baroreceptor unloading, may play a role. The fall in GFR and increase in RVC, which persisted after denervation or when renal perfusion was controlled, implies a local dilatatory influence acting preferentially on the efferent arterioles.It is recognized that systemic hypoxia can have pronounced effects on renal function. However, these effects are controversial. For example, systemic hypoxia has been reported to induce antidiuresis and antinatriuresis in anaesthetized dogs (Anderson et at.

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“…In humans, for example, hypoxia has been reported to cause diuresis and natriuresis [34] or to cause antidiuresis and antinatriuresis [35]. Similarly, in rats, diuresis and natriuresis [36] or antidiuresis and antinatriuresis [37] have been described. However, more recent evidence suggests that acute hypoxia in rats causes antidiuresis and antinatriuresis [38,39] and that chronic hypoxia results in normal renal function [40].…”

Section: Discussionmentioning

confidence: 99%

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

McGuire

Bradford

2001

Eur Respir J

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Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats. M. McGuire, A. Bradford. #ERS Journals Ltd 2001. ABSTRACT: Sleep-disordered breathing is associated with pulmonary hypertension and raised haematocrit. The multiple episodes of apnoea in this condition cause chronic intermittent hypoxia and hypercapnia but the effects of such blood gas changes on pulmonary pressure or haematocrit are unknown. The present investigation tests the hypothesis that chronic intermittent hypercapnic hypoxia causes increased pulmonary arterial pressure and erythropoiesis.Rats were treated with alternating periods of normoxia and hypercapnic hypoxia every 30 s for 8 h per day for 5 days per week for 5 weeks, as a model of the intermittent blood gas changes which occur in sleep-disordered breathing in humans. Haematocrit, red blood cell count and haemoglobin concentration were measured each week and systemic and pulmonary arterial blood pressure and heart weight were measured after 5 weeks.In relation to control, chronic intermittent hypercapnic hypoxia caused a significant increase in systemic (104.3¡4.7 mmHg versus 121.0¡10.4 mmHg) and pulmonary arterial pressure (20.7¡6.8 mmHg versus 31.3¡7.2 mmHg), right ventricular weight (expressed as ratios) and haematocrit (45.2¡1.0% versus 51.5¡1.5%).It is concluded that the pulmonary hypertension and elevated haematocrit associated with sleep-disordered breathing is caused by chronic intermittent hypercapnic hypoxia. Sleep disordered breathing affects 1-4% of adults [1]. It is associated with multiple episodes of hypoxia and hypercapnia due to hypopnoea or apnoea, which are either caused by intermittent collapse of the upper airway (UA), termed obstructive sleep apnoea (OSA; the most common form of sleep disordered breathing), or a reduced drive to breath, termed central apnoea [2]. The condition is associated with a number of cardiovascular changes, including increased pulmonary and systemic arterial blood pressure, right ventricular hypertrophy, cardiac arrhythmias and increased haematocrit. Diurnal pulmonary hypertension is present in 17-42% of OSA patients [3][4][5][6][7] and represents a serious threat to long-term outcome in these patients [8]. The cause of pulmonary hypertension in these patients is unknown. During an apnoeic event, pulmonary arterial pressure is acutely increased [9], presumably due to hypoxic pulmonary vasoconstriction, so that repetitive episodes of increased pressure may ultimately give rise to daytime pulmonary hypertension [10]. In support of this, it has recently been shown that chronic intermittent hypocapnic hypoxia in rats causes right ventricular hypertrophy, suggesting that pulmonary arterial pressure is increased [11]. However, apnoeas are accompanied by hypercapnia as well as hypoxia [12], but the effects of this combination of chronic intermittent blood gas changes on pulmonary arterial pressure are unknown. It is known that chronic continuous hypercapnia protects against the effects of continuous hypoxia...

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Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

Cited by 14 publications

References 0 publications

The role of the renin‐angiotensin system in the renal response to moderate hypoxia in the rat.

The role of the renin‐angiotensin system in the renal response to moderate hypoxia in the rat.

The effects of systemic hypoxia on renal function in the anaesthetized rat.

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

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