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

Neylon, M; Marshall, Janice M.; Johns, Edward J.

doi:10.1113/jphysiol.1996.sp021232

Cited by 23 publications

(33 citation statements)

References 24 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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]. Therefore, it is believed that a decrease in plasma volume is an unlikely contributor to the increased haematocrit in the present experiments.…”

Section: Discussionmentioning

confidence: 44%

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

McGuire

Bradford

2001

Eur Respir J

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionmentioning

confidence: 44%

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

McGuire

Bradford

2001

Eur Respir J

View full text Add to dashboard Cite

show abstract

“…In response to hypoxia, peripheral chemoreceptors are activated and via central pathways a reflex increase in RSNA is induced, as we and others (7,21,27,30,35) have previously observed (18,34,35). Previously, we have demonstrated an increase in RSNA and a fall in RBF (ϳ25%) but maintenance of GFR in response to 14% O 2 (7,21,27,30,35).…”

Section: Discussionmentioning

confidence: 94%

Predominant postglomerular vascular resistance response to reflex renal sympathetic nerve activation during ANG II clamp in rabbits

Denton

Shweta

Flower

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

. Predominant postglomerular vascular resistance response to reflex renal sympathetic nerve activation during ANG II clamp in rabbits. Am J Physiol Regul Integr Comp Physiol 287: R780 -R786, 2004. First published June 10, 2004 10.1152/ ajpregu.00202.2004.-We have shown previously that a moderate reflex increase in renal sympathetic nerve activity (RSNA) elevated glomerular capillary pressure, whereas a more severe increase in RSNA decreased glomerular capillary pressure. This suggested that the nerves innervating the glomerular afferent and efferent arterioles could be selectively activated, allowing differential control of glomerular capillary pressure. A caveat to this conclusion was that intrarenal actions of neurally stimulated ANG II might have contributed to the increase in postglomerular resistance. This has now been investigated. Anesthetized rabbits were prepared for renal micropuncture and RSNA recording. One group (ANG II clamp) received an infusion of an angiotensin-converting enzyme inhibitor (enalaprilat, 2 mg/kg bolus plus 2 mg ⅐ kg, the other vehicle. Measurements were made before (room air) and during 14% O2. Renal blood flow decreased less during ANG II clamp compared with vehicle [9 Ϯ 1% vs. 20 Ϯ 4%, interaction term (PGT) Ͻ 0.05], despite a similar increase in RSNA in response to 14% O2 in the two groups. Arterial pressure and glomerular filtration rate were unaffected by 14% O2 in both groups. Glomerular capillary pressure increased from 33 Ϯ 1 to 37 Ϯ 1 mmHg during ANG II clamp and from 33 Ϯ 2 to 35 Ϯ 1 mmHg in the vehicle group before and during 14% O 2, respectively (PGT Ͻ 0.05). During ANG II clamp, postglomerular vascular resistance was still increased in response to RSNA during 14% O 2, demonstrating that the action of the renal nerves on the postglomerular vasculature was independent of the renin-angiotensin system. This further supports our hypothesis that increases in RSNA can selectively control pre-and postglomerular vascular resistance and therefore glomerular ultrafiltration. kidney; renal innervation; glomerular capillary pressure; renal micropuncture; hypoxia ALTERATIONS in renal sympathetic nerve activity (RSNA) produce several effects on renal function that contribute to the kidneys main task of homeostatic regulation of body fluid balance. Previously, we have identified ultrastructurally two distinct nerve types that are differentially distributed to afferent and efferent arterioles (24,25). Type I axons almost exclusively innervate the afferent arteriole, whereas type II axons are evenly distributed on both arterioles (25). Recently, we have shown that neuropeptide Y (NPY) is located in type II axon terminals but not type I axon terminals (23). Our findings are in accord with the study of Reinecke and Forssmann (38), who reported that the density of NPY-positive terminals was similar on the afferent and efferent arterioles (i.e., similar to type II axon distribution). Taken together, these findings implied that type I and II axons originated from different populations of...

show abstract

“…Chronic hypoxia regulates the expression of RAS in a number of tissues, including the kidney (Neylon et al 1996), the lung (Zhao et al 1996), the heart (Morrell et al 1997) and the pancreas (Chan et al 2000). In the carotid body, Ang II-binding sites have been demonstrated by in vitro autoradiography (Allen 1998).…”

Section: Discussionmentioning

confidence: 99%

Chronic hypoxia upregulates the expression and function of AT(1) receptor in rat carotid body

Leung¹,

Sy²,

Fung³

2000

Journal of Endocrinology

View full text Add to dashboard Cite

In the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT 1 and AT 2 , in the carotid body. The mRNA expression for subtypes of the AT 1 receptor, AT 1a and AT 1b , was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT 1 receptor, an immunohistochemical study was performed. The results showed that AT 1 receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT 1 receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT 1 receptors in the rat carotid body. The upregulation of the expression also enhances AT 1 receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.

show abstract

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

Cited by 23 publications

References 24 publications

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

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

Predominant postglomerular vascular resistance response to reflex renal sympathetic nerve activation during ANG II clamp in rabbits

Chronic hypoxia upregulates the expression and function of AT(1) receptor in rat carotid body

Contact Info

Product

Resources

About