Functions of the Renal Nerves

Koepke, J P; DiBona, Gerald F.

doi:10.1007/978-1-4612-5284-9_9

Cited by 72 publications

(87 citation statements)

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“…Activation of the renal ␣-adrenergic receptors is thought to induce sodium retention through activation of the renin-angiotensin-aldos-terone system causing renal constriction (altering glomerular filtration rate) and/or altering the tubular re-absorption of sodium. 11 Thus, if exaggerated FBF reactivity to mental challenge is in part due to a renal vasoconstrictor response then FBF reactors should also display sodium retention. However, no research as yet has examined this relationship.…”

Section: Journal Of Human Hypertensionmentioning

confidence: 99%

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

Hamer

Boutcher

2002

J Hum Hypertens

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The objective of this study was to compare FBF and renal responses to mental challenge in highly and moderately active males with a family history of hypertension. Normotensive, healthy males with a family history of hypertension (n = 18) were recruited into moderately active and highly active groups. Cardiovascular, FBF, and renal responses to a 10-min Stroop mental challenge were measured. Urine was analysed for levels of sodium and potassium pre and post stressor as an indicant of renal blood flow. The results were that the moderately active males demonstrated a significantly higher level of FBF reactivity to mental challenge compared with that of the highly active. Heart rate change and FBF

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Section: Journal Of Human Hypertensionmentioning

confidence: 99%

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

Hamer

Boutcher

2002

J Hum Hypertens

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“…The renal nerves are known to influence several kidney functions (3,24), including blood flow distribution (11,12). During intensive sympathetic stimulation, such as cold exposure or exhausting exercise, catecholamines may alter renal blood flow and total glomerular filtration rate (11,12).…”

Section: Discussionmentioning

confidence: 99%

“…These differences are mediated in part by sympathetic neural control since the renal vasculature and other parts of the nephron receive extensive noradrenergic innervation (1). Moreover, the kidney presents a high concentration of adrenergic receptors (1)(2)(3)(4) and, based on pharmacological and molecular techniques, the expression of the α-and ß-adrenergic receptor subtypes has been observed in the different regions of the nephron (5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Heterogeneity of glomerular perfusion and filtration induced by epinephrine and norepinephrine

Boim

Stella

Pereira

et al. 1997

Braz J Med Biol Res

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The role of catecholamines in the distribution of intrarenal blood flow and in single-nephron glomerular filtration rate (SNGFR) was evaluated in anesthetized Wistar rats by the Hanssen technique. Epinephrine (EPI) and norepinephrine (NOR) were infused to produce elevations of 20-30 mmHg in mean arterial pressure. Superficial and juxtamedullary nephron perfusion and filtration were determined by the presence of Prussian blue dye. In the control group, 100% of the nephrons presented a homogeneous pattern of perfusion and filtration. In contrast, a heterogeneous distribution of the dye was found even in the larger arteries (arciform and radial), indicating variable perfusion and filtration in both superficial and juxtamedullary nephrons. The effects of EPI and NOR were also evaluated in the superficial cortex by the micropuncture technique in two additional groups of MunichWistar rats. Mean SNGFR was 27% and 54% lower in the EPI-and NOR-treated groups, respectively. No change in mean intraglomerular hydraulic pressure was observed after EPI or NOR infusion in spite of a highly scattered pattern, indicating an important variability in perfusion along the superficial cortex, and/or different sensitivity of the preand post-glomerular arterioles. The present data suggest that EPI and NOR may affect intrarenal hemodynamics by modifying perfusion and filtration in both superficial and juxtamedullary glomeruli and not by shifting blood flow from superficial to juxtamedullary nephrons. The heterogeneous pattern of perfusion was a consequence of differential vasoconstriction along the intrarenal arteries, probably due to different density and/or sensitivity of the adrenergic receptor subtypes present in the intrarenal vascular tree.

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“…Because in that study the aortic resistance was not measured and the degree of constriction of the aorta was monitored by keeping the distal pressure to the occlusion at a fixed level (50 mmHg), this observation was confirmed more recently (17) in conscious intact or bilaterally nephrectomized rats by measuring the change in aortic flow with a pulsed Doppler flowmeter, a technique that provides a reliable measurement of the change in aortic resistance. Nevertheless, removal of the kidneys eliminates hypertensive mechanisms other than the reninangiotensin system (RAS), such as R 2 renal chemoreceptors which are activated by reduction of renal blood flow and by changes in the interstitial ionic environment (18)(19)(20). In addition, it has been reported that in anesthetized rats afferent information from the kidneys selectively alters the activity of vasopressin (AVP) neurosecretory cells of the hypothalamus (supraoptic cells) and may contribute to a reflex pathway through which the kidneys may alter the release of AVP (21,22).…”

Section: Mechanical Vs Renal Factormentioning

confidence: 99%

Vasopressor mechanisms in acute aortic coarctation hypertension

Hc¹,

R²,

Mc³

1997

Braz J Med Biol Res

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Angiotensin II (ANG II) and vasopressin (AVP) act together with the mechanical effect of aortic constriction in the onset of acute aortic coarctation hypertension. Blockade of ANG II and AVP V 1 receptors demonstrated that ANG II acts on the prompt (5 min) rise in pressure whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation during aortic coarctation. Hormone assays carried out on blood collected from conscious rats submitted to aortic constriction supported a role for ANG II in the early stage and a combined role for both ANG II and AVP in the maintenance of proximal hypertension. As expected, a role for catecholamines was ruled out in this model of hypertension, presumably due to the inhibitory effect of the sinoaortic baroreceptors. The lack of afferent feedback from the kidneys for AVP release from the central nervous system in rats with previous renal denervation allowed ANG II to play the major role in the onset of the hypertensive response. Median eminence-lesioned rats exhibited a prompt increase in proximal pressure followed by a progressive decline to lower hypertensive levels, revealing a significant role for the integrity of the neuroaxis in the maintenance of the aortic coarctation hypertension through the release of AVP. In conclusion, the important issue raised by this model of hypertension is the likelihood of a link between some vascular territory -probably renal -below the coarctation triggering the release of AVP, with this vasoconstrictor hormone participating with Ang II and the mechanical effect of aortic constriction in the acute aortic coarctation hypertension. Key words Mechanical vs renal factorFor a long time two schools of thought have attributed different mechanisms to chronic aortic coarctation hypertension. Whereas one school suggested that the mechanical effect of aortic constriction was the main factor promoting high blood pressure (1-3), others (4-6) argued that a renal factor was involved in the arterial pressure elevation. However, it was only in 1968 (7) that studies on young dogs with hypertension induced by chronic aortic coarctation hypertension provided a clear-cut demonstration that both factors, i.e., mechanical and renal factors, were operative in this model for hypertension. Later, these observations were confirmed in adult dogs submitted to aortic constriction, indicating a major role for the renal mechanisms in the development of hypertension, associated with a role played by aortic constriction (8).

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Functions of the Renal Nerves

Cited by 72 publications

References 0 publications

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

Heterogeneity of glomerular perfusion and filtration induced by epinephrine and norepinephrine

Vasopressor mechanisms in acute aortic coarctation hypertension

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