Dissociation between changes in renal nerve activity and renal vascular resistance in conscious dogs.

Morita, Hironobu

doi:10.2170/jjphysiol.36.585

Cited by 9 publications

(3 citation statements)

References 21 publications

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“…Morita reported that RBF (Doppler flowmetry) was unchanged by reductions in RSNA of 18–87% during blood volume expansion. 48,53 None of the above experiments found that renal haemodynamics changed despite producing sustained increases in RSNA.…”

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

confidence: 90%

“… 47 Similarly, non‐hypotensive haemorrhage, although increasing RSNA by 76%, did not alter RBF (assessed by Doppler flowmeter). 48 In another study, two levels of non‐hypotensive haemorrhage produced a graded increase in RSNA of 40 and 52%, increased PRA and decreased sodium excretion in a step‐wise fashion, but did not change RBF (assessed by electromagnetic flowmetry). 49 These observations are also consistent with those studies in which RSNA was increased using carotid occlusion but renal perfusion pressure was servo‐controlled.…”

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

confidence: 96%

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Neural Regulation Of Renal Blood Flow: A Re‐Examination

Malpas

Leonard

2000

Clin Exp Pharma Physio

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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...

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

confidence: 90%

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

confidence: 96%

Neural Regulation Of Renal Blood Flow: A Re‐Examination

Malpas

Leonard

2000

Clin Exp Pharma Physio

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“…Furthermore, the latter recordings were only functional for a few postoperative days. This limitation, confirmed by Morita (1986), does not allow studies in an atraumatic and unrestrained state which we considered obligatory in order to quantify the effect of CSNS on the renin-angiotensin system. Even a minor surgical trauma increases PRA considerably, besides leading to higher blood pressures than normally observed (Frommer & Ayus 1985) which may counteract the effects of CSNS.…”

Section: Discussionmentioning

confidence: 99%

Plasma Renin Activity During Hypotensive Responses to Electrical Stimulation of Carotid Sinus Nerves in Conscious Dogs

Peters

Kaczmarczyk

1994

Clin Exp Pharma Physio

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1. The interaction of electrical stimulation of the carotid sinus nerves (carotid sinus nerve stimulation, CSNS) with mechanisms of renin release was studied in conscious and unrestrained resting beagle dogs receiving a standardized diet (sodium intake, 4.5 mmol/kg bodyweight (bw); water intake, 91 mL/kg bw). 2. By CSNS, mean arterial blood pressure (MAP) was lowered for periods of 20 min to levels between 101 +/- 4 and 56 +/- 5 mmHg. 3. In another group of conscious dogs, renal perfusion pressure (RPP) was lowered to 95 +/- 4 mmHg for periods of 20 min by partial suprarenal aortic occlusion in order to assess the influence of a reduced RPP on plasma renin activity (PRA) without concomitant CSNS. 4. During CSNS, PRA increased markedly (> 100%) only when MAP was reduced below 75 mmHg. 5. With aortic constriction and an RPP of 95 mmHg, the increase in PRA was 955%, which is more than three-fold higher than the increase in PRA during CSNS at MAP levels < 65 mmHg (314%). 6. The observed responses indirectly support the hypothesis that basal activity in efferent renal nerve discharge is present even at rest and can be inhibited by CSNS, and furthermore suggests that CSNS attenuated the pressure-dependent renin release.

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Neural Control of Renal Function

Moss

Colindres

Gottschalk

1992

Comprehensive Physiology

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The sections in this article are: Current Research Historical Perspective Neuroanatomy and Neurophysiology Efferent Renal Innervation Afferent Renal Innervation Renal Adrenergic Receptors General Concepts Prejunctional Renal Receptors Post‐ and Extrajunctional Adrenoceptors Renal Tubular and Vascular Dopamine Receptors Renal Cholinergic Receptors Cellular Transduction of Neurotransmitter Effects Sympathetic Nervous System and Renal Hemodynamics Vasoconstrictor Responses Vasodilatory Responses Sympathetic Nervous System and Renal Tubular Function Studies in Anesthetized Animals Studies in Conscious Animals Effects of Neurotransmitters on Renal Tubular Function Cellular Mechanisms in the Renal Tubular Responses to Catecholamines Sympathetic Nervous System and Renin Secretion by the Kidney General Concepts Effects of Direct and Reflex Stimulation of the Renal Nerves Effects of Renal Denervation on Renin Release Renal Adrenoceptors Involved in Renin Secretion Interactions Between Nerves and Prostaglandins in Renin Release

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Dissociation between changes in renal nerve activity and renal vascular resistance in conscious dogs.

Cited by 9 publications

References 21 publications

Neural Regulation Of Renal Blood Flow: A Re‐Examination

Neural Regulation Of Renal Blood Flow: A Re‐Examination

Plasma Renin Activity During Hypotensive Responses to Electrical Stimulation of Carotid Sinus Nerves in Conscious Dogs

Neural Control of Renal Function

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