Renal nerve stimulation causes alpha 1-adrenoceptor-mediated sodium retention but not alpha 2-adrenoceptor antagonism of vasopressin.

Smyth, Donald D.; Umemura, Satoshi; Pettinger, William A.

doi:10.1161/01.res.57.2.304

Cited by 60 publications

(34 citation statements)

References 26 publications

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“…This relationship is by no means proven by the present studies; however, it is recognised that the major reabsorption pathway for calcium ions at these sections of the nephron is via the sodium/potassium ATPase-driven sodium/calcium counter transporter system at the basolateral membranes of the tubular cells (Katz, 1986 The results of the present study also indicated that x1-adrenoceptors were necessary for the activation of tubular sodium reabsorption as renal nerve stimulation in the presence of prazosin did not change sodium output whereas during administration ofidazoxan the magnitude of the increases in tubular sodium reabsorption were similar to those in the animals receiving only saline. A role for a1-adrenoceptors in the adrenergic stimulation of tubular sodium reabsorption in the rat was recently reported in in vitro studies by Smyth et al (1985) and the present study using in vivo experiments support these in vitro findings. It is becoming apparent that this particular end-point of adrenergic activity within the kidney also requires ax-adrenoceptors in the rabbit (Hesse & Johns, 1984a; and the dog (Osborn et al, 1983).…”

Section: Discussionsupporting

confidence: 90%

An investigation into the α‐adrenoceptor mediating renal nerve‐induced calcium reabsorption by the rat kidney

Johns

Manitius

1986

British J Pharmacology

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1 An investigation was undertaken in pentobarbitone-anaesthetized rats to determine the sub-type of a-adrenoceptor responsible for the renal nerve-induced increases in the reabsorption of calcium and sodium by the tubules of the kidney. 2 Stimulation of the renal nerves at low frequencies (0.8-1.5 Hz) did not change either renal blood flow or glomerular filtration rate but significantly reduced urine flow by 32%, calcium excretion by 36% and absolute and fractional sodium excretions by 36% and 22%, respectively. 3 In the presence of the selective m,-adrenoceptor antagonist prazosin, renal nerve stimulation (2-3 Hz) caused a significant reduction in renal blood flow of 7% but did not change either glomerular filtration rate, urine flow, calcium excretion or absolute and fractional sodium excretions. 4 During administration of the selective c,-adrenoceptor antagonist, idazoxan, renal nerve stimulation (1.0-1.5 Hz) significantly reduced renal blood flow by 4% and glomerular filtration rate by 7%; at the same time there were significant falls in urine flow of43%, calcium excretion of43% and absolute and fractional sodium excretions of 41 % and 37%, respectively. 5 These results show that low frequency renal nerve stimulation causes an anticalciuresis, independent ofrenal haemodynamics, which represents an increase in tubular reabsorption ofcalcium. This effect was blocked by prazosin but not idazoxan which is consistent with the mediation of a,-adrenoceptors. The neurally-induced antinatriuresis also appeared to be dependent on the activation of oc-adrenoceptors.

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Section: Discussionsupporting

confidence: 90%

An investigation into the α‐adrenoceptor mediating renal nerve‐induced calcium reabsorption by the rat kidney

Johns

Manitius

1986

British J Pharmacology

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“…29 Others have demonstrated that sympathetic nerve endings directly release norepinephrine on renal epithelial cells and can cause a 30% to 40% increase in sodium and water reabsorption via α-1 adrenergic receptors even before any hemodynamic changes could be detected. 30,31 …”

Section: Renal Nerves: Efferent and Afferent Sympathetic Fibersmentioning

confidence: 99%

Renal Nerve Ablation for Resistant Hypertension

et al. 2014

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S ympathetic renal denervation, or renal nerve ablation (RNA), has become the new buzz word in hypertension and interventional cardiology. Recent advances in catheterbased approaches have allowed sympathetic fiber interruption through transvascular techniques that are minimally invasive and can be delivered expeditiously and safely. Radiofrequency (RF) energy sources are currently the preferred modalities, but other sources of energy, such as cryoablation, microwave, high-intensity focus ultrasound, and local neurotoxic agent infusion, are under intense investigation. Results thus far have been encouraging and offer promise for the future. The role of the sympathetic nervous system (SNS) in the development of resistant hypertension and cardiovascular disease has long been known, and a great deal of work has been done through the years trying to explore potential interventions to interrupt the sympathetic influence on systemic vasculature and target organs. In this article we attempt an overview of timedependent interventions on the SNS and examine approaches used in humans and in the many experimental models that offer a better understanding of the role of sympathetic activity in cardiovascular disease. Naturally we focus on methods and techniques addressing sympathetic renal denervation in patients with drug-resistant hypertension, examine the current state of the art, and attempt a look into the future. Historic PerspectiveIn 1889, after meticulous experiments on dogs, Bradford 1 reported that stimulation of dorsal and splanchnic nerves causes changes in blood pressure (BP) and kidney size measured by plethysmography. Whether BP increased or decreased depended on the anatomic area stimulated, as well as the electric impulse frequency, but outcomes were consistent and reproducible. Neurosurgical treatment of hypertension was independently suggested by researchers in 1923. Adson, however, was the first to performed surgical sympathectomy for the treatment of malignant hypertension in 1925.3 During the following years and in the 1930s, Peet in Ann Arbor, Page and Heuer in New York, and Adson, Craig, and Brown from the Mayo Clinic operated and reported on series of patients all experiencing malignant hypertension.4 At the same time, renal decapsulation, which was considered a form of sympathectomy by disrupting the fibers between the capsule and the renal cortex, was being performed to treat unexplained hematuria and perinephritis. Sen 5 reported a significant but not permanent decrease in BP in 85 subjects who underwent decapsulation between 1925 and 1935.Surgical denervation of the kidneys alone was first performed in humans by Papin and Ambard 6 in 1924 in an attempt to relieve intractable pain originating from the kidney. The first case of bilateral sympathetic denervation of the kidney to treat severe essential hypertension was presented in 1934 by Page and Heuer. 7 The patient was a 25-year-old woman who reported easy fatigability and had severe headaches and BP in the range of 208/140 mm Hg. The patient und...

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“…In our study, it was unlikely that idazoxan was a partial al-adrenoceptor agonist. This would be expected to decrease urine flow rate and sodium excretion (Smyth et al, 1985) and not increase these parameters as we observed. Goldstein et al (1983) using doses similar to that reported in the present study found that, whereas low doses (0.25 mg kg-') of RX 781094 (idazoxan) suppressed nerve firing in the locus coeruleus, a slightly higher dose (1.0 mg kg-1) increased the firing rate.…”

Section: Resultsmentioning

confidence: 50%

Antagonism by idazoxan at low dose but not high dose, of the natriuretic action of moxonidine

Allan

Penner

Smyth

1996

British J Pharmacology

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1 Recent studies concerning the imidazoline receptor have utilized idazoxan as a specific imidazoline receptor antagonist. The aim of the present study was to describe the in vivo effects of various doses of idazoxan on renal function, in the presence and absence of moxonidine, an I, imidazoline receptor agonist. 2 In anaesthetized, unilaterally nephrectomized (7 to 10 days) Sprague Dawley rats, an intrarenal infusion of moxonidine (3 nmol kg-' min-') increased urine flow rate, sodium excretion and osmolar clearance without altering free water clearance. Pretreatment with intravenous idazoxan at 0.1 and 0.3 mg kg-' produced a dose-related decrease in the renal actions of moxonidine. However, a higher dose of idazoxan (1 mg kg-') was not as effective as the 0.3 mg kg-' dose in blocking the effects of moxonidine.3 In a separate series of experiments, the direct renal actions of idazoxan alone were investigated. Idazoxan at 0.3 mg kg-' failed to alter urine flow rate and sodium excretion. However, idazoxan at 1 mg kg-' produced a significant increase in urine flow rate and sodium excretion in association with an increase in osmolar clearance. 4 These results do not prove but are consistent with low doses of idazoxan antagonizing the sites stimulated by moxonidine (renal imidazoline receptors). However, at higher doses, idazoxan may function as a partial agonist and/or interact with other receptors to increase urine flow rate, independent of imidazoline receptor blockade. These studies underscore the importance of the dose of idazoxan administered when this antagonist is used as a tool to investigate imidazoline receptors.

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Renal nerve stimulation causes alpha 1-adrenoceptor-mediated sodium retention but not alpha 2-adrenoceptor antagonism of vasopressin.

Cited by 60 publications

References 26 publications

An investigation into the α‐adrenoceptor mediating renal nerve‐induced calcium reabsorption by the rat kidney

An investigation into the α‐adrenoceptor mediating renal nerve‐induced calcium reabsorption by the rat kidney

Renal Nerve Ablation for Resistant Hypertension

Antagonism by idazoxan at low dose but not high dose, of the natriuretic action of moxonidine

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