Primary neural involvement in renal haemodynamic and functional responses to prolonged stimulation of atrial receptors in anaesthetized dogs

Majid, Dewan S. A.; Karim, Fazlul

doi:10.1113/expphysiol.1995.sp003873

Cited by 4 publications

(5 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results are contrary to those in conscious monkeys, in which the renal response to volume loading is abolished by renal denervation (Peterson, Chase & Gray, 1984). They are also contrary to the results obtained in dogs subjected to head-out immersion (Miki, Hayshida, Sagawa & Shiraki, 1989 (Majid & Karim, 1995) (1995), as in our chronic preparation, also used chloralose. On the other hand, Emmeluth, Goetz, Drummer, Gerzer, Forssmann & Bie (1993) recently reported a persistent natriuresis in conscious trained dogs with renal denervation when isotonic volume expansion was carried out over 100min.…”

Section: Discussioncontrasting

confidence: 99%

“…Curiously, head-out immersion natriuresis is preserved in humans with denervated kidneys (Rabelink, van Tilborg, Hene & Koomans, 1993), but not in the dogs of Miki et al (1989); our dogs seem to have responses that are more consonant with the results obtained in human subjects. A recent acute study also suggests that renal denervation abolishes atrial natriuresis (Majid & Karim, 1995); in this study acute denervation increased basal sodium excretion but the increase with balloon dilatation of the pulmonary vein/left atrial junctions was blocked. It is possible that no further increase could take place because of maximal basal excretion.…”

Section: Discussionsupporting

confidence: 45%

“…It is of interest that Peterson, Benjamin & Hurst (1988) also obtained a response if their monkeys were anaesthetized. However, Majid & Karim (1995), as in our chronic preparation, also used chloralose. On the other hand, Emmeluth, Goetz, Drummer, Gerzer, Forssmann & Bie (1993) recently reported a persistent natriuresis in conscious trained dogs with renal denervation when isotonic volume expansion was carried out over 100min.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Drake-Holland¹,

Song²,

Belcher³

et al. 1996

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYThe influence of renal denervation on the renal response to rapid blood volume expansion was investigated by measurement of urine volume, sodium and osmolar excretion rates, sodium p-aminohippurate and free water clearances, and systemic haemodynamic and plasma hormone (atrial natriuretic peptide, arginine vasopressin and plasma renin activity (PRA)) changes in ten control and ten renal-denervated chloralose-anaesthetized mongrel dogs. Following renal denervation, blood volume expansion caused a similar increase in sodium excretion to that in the control group. Renal denervation resulted in systemic vasodilatation and decreased PRA. During fluid loading the right atrial pressure and pulmonary capillary wedge pressure were significantly higher in the control group. In the control group, volume expansion caused a large fall in PRA, whereas in the renal-denervated dogs, PRA remained suppressed. We conclude, from the fact that natriuresis is preserved after renal denervation, that this response is not mediated by a reflex with efferent limb in the renal nerves.

show abstract

Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Drake-Holland¹,

Song²,

Belcher³

et al. 1996

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…However, there are conflicting studies in dogs that do indicate that renal nerves can regulate RBF. Majid and Karim 54 compared RBF responses in renal nerve‐intact and ‐denervated kidneys within the same anaesthetized dog during stimulation of left atrial receptors. By carefully preventing changes in blood pressure, they found RBF increased by 6% and this was renal nerve dependent.…”

Section: Steady State Control Of Renal Haemodynamics By the Renal Nervesmentioning

confidence: 99%

Neural Regulation Of Renal Blood Flow: A Re‐Examination

Malpas

Leonard

2000

Clin Exp Pharma Physio

View full text Add to dashboard Cite

SUMMARY1. The importance of renal sympathetic nerve activity (RSNA) in the regulation of renal function is well established. However, it is less clear how the renal vasculature responds to the different mean levels and patterns of RSNA. While many studies have indicated that small to moderate changes in RSNA preferentially regulate renin secretion or sodium excretion and only large changes in RSNA regulate renal blood flow (RBF), other experimental evidence suggests that small changes in RSNA can influence RBF 2. When RSNA has been directly measured in conjunction with RBF, it appears that a range of afferent stimuli can induce reflex changes in RBF. However, many studies in a variety of species have measured RBF only during stimuli designed to reflexly increase or decrease sympathetic activity, but have not recorded RSNA. While this approach can be informative, it is not definitive because the ability of the vasculature to respond to RSNA may, in part, reflect the resting level of RSNA and, therefore, the vasoconstrictive state of the vasculature under the control conditions.3. Further understanding of the control of RBF by RSNA has come from studies that have analysed the underlying rhythms in sympathetic nerve activity and their effect on the cardiovascular system. These studies show that the frequency-response characteristic of the renal vasculature is such that higher frequency oscillations in RSNA (above 0.6 Hz) contribute to setting the mean level of RBF. In comparison, lower frequency oscillations in RSNA can induce cyclic vasoconstriction and dilation in the renal vasculature, thus inducing oscillations in RBF.4. In summary, the present review discusses the neural control of RBF, summarizing evidence in support of the hypothesis that RBF is under the influence of RSNA across the full range of RSNA.Key words: oscillations, spectral analysis, sympathetic nervous system. INTRODUCTIONUnder resting conditions, renal blood flow (RBF) accounts for approximately 20% of cardiac output; thus, its regulation is fundamental to the control of blood pressure. Despite this, many aspects of the regulation of RBF have not been fully determined, especially the role of the renal sympathetic innervation. The influence of renal sympathetic nerve activity (RSNA) on RBF has been thought to be restricted to very high levels of activation, as described by the 'fight or flight' response.1 Small to moderate changes in RSNA have been proposed to preferentially regulate renin secretion or sodium excretion so that renal haemodynamics are altered 2 only at high levels of nerve activity. The present paper reviews evidence contrary to this view, especially recent evidence suggesting a role for the sympathetic nerves in the regulation of RBF during small changes in RSNA, which, it is argued, are relevant to those occurring in 'daily life'. More recent analysis of changes in RBF around normal resting levels also indicates a role for RSNA in the dynamic control of renal haemodynamics.The present review is divided into two parts: (i) a rev...

show abstract

“…Although indirect measurements suggest that RSNA has some effect on renal blood flow in humans, such an effect is controversial in dogs (43). In dogs, RSNA is generally known to have no effect on renal blood flow, but the reverse has also been demonstrated (42). When the blood pressure changes were prevented and the left atrium was simultaneously stimulated, renal blood flow increased in the innervated kidney, but there was no change in renal blood flow in the denervated kidney (42).…”

Section: Simulation Results and Discussionmentioning

confidence: 99%

A mathematical model of long-term renal sympathetic nerve activity inhibition during an increase in sodium intake

Karaaslan

Denizhan

Hester

2014

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

It is well known that renal nerves directly affect renal vascular resistance, tubular sodium reabsorption, and renin secretion. Inhibition of renal sympathetic nerve activity (RSNA) decreases renal vascular resistance, tubular sodium reabsorption, and renin secretion, leading to an increase in sodium excretion. Although several studies show that inhibition of RSNA promotes sodium excretion during an acute blood volume expansion, there is limited research relating to the importance of RSNA inhibition that contributes to sodium homeostasis during a long-term increase in sodium intake. Therefore, to dissect the underlying mechanisms of sodium excretion, a mathematical model of a cardiovascular system consisting of two kidneys, each with an independent RSNA, was developed. Simulations were performed to determine the responses of RSNA and sodium excretion to an increased sodium intake. In these simulations, RSNA in the left kidney was fixed at its normal steady-state value, while RSNA in the contralateral kidney was allowed to change normally in response to the increased sodium intake. The results demonstrate that the fixed-RSNA kidney excretes less sodium than the intact-RSNA collateral kidney. Because each kidney is exposed to the same arterial pressure and circulatory hormones, the impaired sodium excretion in the absence of RSNA inhibition supports the hypothesis that RSNA inhibition contributes to natriuresis in response to a long-term increase in sodium intake.

show abstract

Primary neural involvement in renal haemodynamic and functional responses to prolonged stimulation of atrial receptors in anaesthetized dogs

Cited by 4 publications

References 24 publications

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Neural Regulation Of Renal Blood Flow: A Re‐Examination

A mathematical model of long-term renal sympathetic nerve activity inhibition during an increase in sodium intake

Contact Info

Product

Resources

About