The cortical and medullary blood flow at different levels of renal nerve activity

Hermansson, Kersti; Öjteg, G.; Wolgast, M.

doi:10.1111/j.1748-1716.1984.tb00121.x

Cited by 34 publications

(27 citation statements)

References 33 publications

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“…Some early studies used 85 Kr autoradiography (24) or 86 Rb uptake (12), methods that allow some distinctions to be made across anatomic regions. These studies suggested variously that MBF is more sensitive than CBF to neural activation (12) or that renal nerve stimulation can increase MBF (24). Regardless, these studies should be interpreted with great care, because the validity of their methodology has been questioned (11,23).…”

Section: Discussionmentioning

confidence: 99%

Regional responsiveness of renal perfusion to activation of the renal nerves

Guild

Eppel

Malpas

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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We tested for regional differences in perfusion responses, within the renal medulla and cortex, to renal nerve stimulation in pentobarbital sodium-anesthetized rabbits. Laser-Doppler flux (LDF) was monitored at various depths below the cortical surface (1–15 mm). Basal cortical LDF (1–3 mm, ∼200–450 U) was greater than medullary LDF (5–15 mm, ∼70–160 U), but there were no statistically significant differences in basal LDF within these regions. The background LDF signal during aortic occlusion was similar in the cortex (2 mm, 31 U) and outer medulla (7 mm, 31 U), but slightly greater in the inner medulla (12 mm, 44 U). During electrical stimulation of the renal nerves (0.5–8 Hz), cortical LDF and total renal blood flow were similarly progressively reduced with increasing stimulus frequency. Medullary LDF (measured between 5 and 15 mm) was overall less responsive than cortical LDF. For example, 4-Hz stimulation reduced inner medullary LDF (9 mm) by 19 ± 6% but reduced cortical LDF (1 mm) by 54 ± 11%. However, medullary LDF responses to nerve stimulation were similar at all depths measured. Our results indicate that while the vascular elements controlling medullary perfusion are less sensitive to the effects of electrical stimulation of the renal nerves than are those controlling cortical perfusion, sensitivity within these vascular territories appears to be relatively homogeneous.

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Section: Discussionmentioning

confidence: 99%

Regional responsiveness of renal perfusion to activation of the renal nerves

Guild

Eppel

Malpas

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The vasculature of the renal medulla has been reported to have greater adrenergic tone than that of the cortex 16 ; thus, to protect this region of the kidney from excessive vasoconstriction, it may require a stronger counterregulatory system. The NO system in the renal medulla has been shown to be an effective counterregulatory mechanism against the vasoconstrictor actions of angiotensin II and vasopressin.…”

Section: Ne Stimulation Of Renal Medullary Nos Activitymentioning

confidence: 99%

Increase in Renal Medullary Nitric Oxide Synthase Activity Protects From Norepinephrine-Induced Hypertension

et al. 2000

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Abstract-Studies were performed in conscious Sprague-Dawley rats to determine the role of the ␣ 2 -adrenergic receptor-mediated increase in the renal medullary nitric oxide synthase (NOS) activity as a counterregulatory mechanism of blood pressure control in response to increased renal adrenergic stimulation. A subpressor dose of norepinephrine (NE, 8 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) was infused intravenously, and NOS activity was determined with arginine-citrulline conversion by high-performance liquid chromatography in renal cortical and outer and inner medullary tissues. It was found that after 7 days of intravenous NE infusion, NOS activity was significantly higher in both the outer and inner medullary tissues (158Ϯ45 versus 30Ϯ24 pmol ⅐ mg Ϫ1 ⅐ h Ϫ1 [outer medulla] and 5.1Ϯ0.7 versus 2.0Ϯ0.5 nmol ⅐ mg Ϫ1 ⅐ h Ϫ1 [inner medulla] for NE-treated versus control rats, respectively). To determine whether the increase of NOS activity was mediated through renal medullary ␣ 2 -receptors, the receptor antagonist rauwolscine (RAU, 1 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ) was infused via an implanted renal medullary interstitial catheter, and the consequences of intravenous NE administration were evaluated. NOS activity was significantly lower in the RAU-infused animals and did not increase with infusion of NE. To determine the systemic effects of the renal medullary ␣ 2 -receptors, studies were performed to determine the consequences of chronic intravenous infusion of subpressor amounts of NE in the presence and absence of renal medullary ␣ 2 -receptor inhibition. Under conditions in which RAU was continuously infused into the renal medulla, the same subpressor dose of NE caused sustained and reversible hypertension (mean arterial pressure increased from 120Ϯ3 to 131Ϯ3 mm Hg). Chronic blunting of the renal medullary NOS activity with N G -nitro-L-arginine methyl ester (75 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) also enabled NE to produce a significant rise in mean arterial pressure (from 117Ϯ2 to 134Ϯ4 mm Hg). We conclude that the hypertensive effects of moderate elevations of renal adrenergic activity were chronically buffered by the ␣ 2 -receptor-mediated increase in NOS activity within the renal medulla. Key Words: norepinephrine Ⅲ receptors, adrenergic, alpha Ⅲ rauwolscine Ⅲ nitric oxide synthase Ⅲ rats I t has been found that small subpressor amounts of intravenously infused norepinephrine (NE) can stimulate renal medullary nitric oxide concentration ([NO]) in anesthetized Sprague-Dawley rats. 1 This NE-stimulated medullary nitric oxide (NO) release significantly counteracted the medullary vasoconstrictor actions of NE, suggesting an important counterregulatory role of the adrenergic-NO interactions. Sai et al 2 showed that in isolated perfused outer medullary vasa recta, N G -nitro-L-arginine methyl ester (L-NAME) increased the NE response. These observations are of relevance to the longterm control of arterial blood pressure 3 because the renal medullary circulation plays an important role in the mechanism of pressure natriuresis. 4 -7 Chronic reductions of blood ...

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“…32 Plasma levels of vasopressin, angiotensin, atrial natriuretic factor, and renal nerve activity are all affected by changes in blood volume. To determine whether the efficiency of papillary blood flow autoregulation is altered by changes in the level of hydration, experiments were performed in hydropenic rats.…”

mentioning

confidence: 99%

Pressure-diuresis in volume-expanded rats. Cortical and medullary hemodynamics.

et al. 1988

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SUMMARY This study evaluated whether pressure-diuretic and pressure-natriuretlc responses are associated with alterations in vasa recta hemodynamics. Autoregulation of cortical and papillary blood flow was studied using a laser-DoppIer flowmeter in volume-expanded and hydropenk rats. Superficial cortical flow and whole kidney renal blood flow were antoregulated in volume-expanded rats and decreased by less than 10% after renal perfusion pressure was lowered from 150 to 100 mm Hg. In contrast, papillary blood flow was not autoregulated and fell by 24 ± 2%. The failure of papillary blood flow to autoregulate was due to changes in the number of perfused vessels as well as to alterations In blood flow in individual ascending and descending vasa recta. Pressure hi vasa recta capillaries increased from 6.8 ± 0.8 to 13.8 ± 1.2 mm Hg after renal perfusion pressure was elevated from 100 to 150 mm Hg, and renal Interstitial pressure rose from 7.4 ± 0.8 to 12.3 ± 1.4 mm Hg. In hydropenic rats, papillary blood flow was autoregulated to a significant extent, but it still decreased by 19% after renal perfusion pressure was lowered from 150 to 100 mm Hg. The pressure-diuretic and presure-natriuretic responses in hydropenic rats were blunted in comparison to those observed in volume-expanded rats.

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The cortical and medullary blood flow at different levels of renal nerve activity

Cited by 34 publications

References 33 publications

Regional responsiveness of renal perfusion to activation of the renal nerves

Regional responsiveness of renal perfusion to activation of the renal nerves

Increase in Renal Medullary Nitric Oxide Synthase Activity Protects From Norepinephrine-Induced Hypertension

Pressure-diuresis in volume-expanded rats. Cortical and medullary hemodynamics.

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