Is the chronically denervated kidney supersensitive to  catecholamines?

Ramchandra, Rohit; Barrett, Carolyn J.; Guild, Sarah-Jane; Malpas, Simon C.

doi:10.1152/ajpregu.00404.2001

Cited by 17 publications

(15 citation statements)

References 14 publications

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“…Our finding of NE supersensitivity in isolated interlobar artery segments from sympathectomized SHR, compared with sham-or hydralazine-treated SHR appears to be in contrast with in vivo data obtained in surgically denervated rabbit kidneys, which do not show supersensitivity of the renal blood flow response to the a 1 -adrenoceptor agonist phenylephrine [18]. A potential explanation for this discrepancy may be the different plasma catecholamine concentrations in these models.…”

Section: Discussioncontrasting

confidence: 96%

Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats

Grisk

Lother

Gabriëls

et al. 2004

Pflugers Arch - Eur J Physiol

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Renal transplantation experiments have shown that the kidney contributes to chronic sympathectomy-induced arterial pressure reduction in spontaneously hypertensive rats (SHR). The underlying mechanisms are currently unclear but may include alterations in the function of small renal arteries. Neonatal SHR were sympathectomized by intraperitoneal guanethidine injections and removal of adrenal medullary tissue. Controls were sham- or hydralazine-treated. At 12 weeks of age, distal interlobar artery segments were investigated using small-vessel wire myography. Vessels from sympathectomized animals showed increased sensitivity to noradrenaline (NE). Vasopressin- and endothelin-1-induced vasoconstriction was similar in all groups (as reflected by the pD(2), i.e. -logEC(50), where EC(50) is the molar concentration of agonist eliciting a half-maximal response). Maximum vasopressin-induced tension was similar in all groups while endothelin-1-induced maximum tension was significantly higher in sympathectomized than in sham-treated SHR. The sensitivity of NE-induced vasoconstriction to extracellular Ca(2+) did not differ between groups while sensitivity to L-type Ca(2+) channel activation was significantly higher in both sympathectomized and hydralazine-treated animals than in sham-treated animals. Endothelium-dependent and independent vasodilation were similar in all groups. Sequential blockade of NO-synthase and cyclooxygenase had similar effects in all groups. In conclusion, neonatal sympathectomy does not induce any changes in the function of isolated proximal renal resistance arteries from SHR that could explain the blood pressure lowering effect of a kidney graft from sympathectomized SHR.

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Section: Discussioncontrasting

confidence: 96%

Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats

Grisk

Lother

Gabriëls

et al. 2004

Pflugers Arch - Eur J Physiol

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“…14,21 More recent studies in animals with an innervated and denervated kidney provide strong evidence that chronically denervated kidneys do not have either exaggerated renal vascular or sodium excretory responses to either physiological or pathophysiological increments in circulating levels of NE. 21,26 It must be emphasized, however, that because of expediency, virtually all of the studies relating to the topic of renal denervation supersensitivity have investigated renal responses to increases, but not decreases, in adrenergic stimulation. Consequently, it is not known whether denervated kidneys are supersensitive to normal circulating levels of NE.…”

Section: Discussionmentioning

confidence: 99%

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Lohmeier

Hildebrandt²,

Dwyer³

et al. 2007

Hypertension

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Abstract-Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean arterial pressure and plasma norepinephrine concentration were 95Ϯ2 mm Hg and 96Ϯ12 pg/mL, respectively. During day 1 of baroreflex activation, mean arterial pressure decreased 13Ϯ1 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean arterial pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with sustained decreases in plasma norepinephrine concentration (Ϸ50%) and plasma renin activity (30% to 40%). All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean arterial pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were comparable to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were similar to those observed before renal denervation. These findings demonstrate that the presence of the renal nerves is not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex. Key Words: baroreflex Ⅲ arterial pressure Ⅲ renal nerves Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ renin-angiotensin system Ⅲ sodium excretion N ovel experimental approaches in chronically instrumented animals have recently provided greater insight into the role of baroreflexes in long-term control of arterial pressure. 1-10 These studies, conducted over several weeks, indicate that baroreflex resetting is incomplete in experimental models of hypertension. They also indicate that during chronic increases in arterial pressure, there is sustained baroreflex-mediated suppression of renal sympathetic nerve activity and attendant increments in renal excretory function, responses expected to attenuate the severity of hypertension. However, the quantitative importance of renal sympathoinhibition in mediating the chronic blood pressure-lowering effects of sustained baroreflex activation remains unclear.We have recently developed methodology that is ideal for evaluating the time dependency and underlying mechanisms of the blood pressure-lowering effects of the baroreflex. 6,10 To activate the carotid baroreflex, an externally adjustable pulse generator is used to electrically stimulate electrodes chronically implanted around both c...

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“…This has been investigated in a number of species and has been a matter of controversy (24,(27)(28)(29)(30). [27][28][29][30].…”

Section: Responsiveness To Vasopressorsmentioning

confidence: 99%

“…This has been investigated in a number of species and has been a matter of controversy (24,(27)(28)(29)(30). [27][28][29][30]. In acutely and chronically denervated rats (24,28) and dogs (27,29), enhanced responsiveness to catecholamines was found.…”

Section: Responsiveness To Vasopressorsmentioning

confidence: 99%

Effects of Renal Denervation on Regional Hemodynamics and Kidney Function in Experimental Hyperdynamic Sepsis

Calzavacca

Bailey

Velkoska

et al. 2014

Critical Care Medicine

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Is the chronically denervated kidney supersensitive to catecholamines?

Cited by 17 publications

References 14 publications

Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats

Influence of neonatal sympathectomy on proximal renal resistance artery function in spontaneously hypertensive rats

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Effects of Renal Denervation on Regional Hemodynamics and Kidney Function in Experimental Hyperdynamic Sepsis

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