Influence of renal denervation on blood pressure, sodium and water excretion in acute total obstructive apnea in rats

Franquini, Joao; Medeiros, Ana Raquel Santos; Andrade, Teresa; Araújo, Maria Teresa Martins de; Moysés, Margareth Ribeiro; Abreu, Gláucia Rodrigues de; Vasquez, Elisardo C.; Bissoli, Nazaré Souza

doi:10.1590/s0100-879x2009000200010

Cited by 10 publications

(5 citation statements)

References 39 publications

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“…Burke et al demonstrated that the kidney function appears to be well preserved in animals that have had one kidney clipped and the blood pressure normalized by sympathetic inhibition [ 38 ]. Franquini et al [ 39 ] demonstrated that renal denervation induced an increase in urine volume and sodium excretion. In contrast, DiBona and Sawin [ 26 ] showed that renal denervation prevents the renal vasoconstrictor response and antinatriuresis.…”

Section: Discussionmentioning

confidence: 99%

Role of Renal Nerves in the Treatment of Renovascular Hypertensive Rats withL-Arginine

Gouvêa

Tiradentes

Santuzzi

et al. 2014

International Journal of Hypertension

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The purpose was to determine the role of renal nerves in mediating the effects of antihypertensive treatment with L-arginine in a renovascular hypertension model. The 2K1C (two-kidney one-clip model) hypertensive rats were submitted to bilateral surgical-pharmacological renal denervation. The animals were subdivided into six experimental groups: normotensive control rats (SHAM), 2K1C rats, 2K1C rats treated with L-arginine (2K1C + L-arg), denervated normotensive (DN) rats, denervated 2K1C (2K1C + DN) rats, and denervated 2K1C + L-arg (2K1C + DN + L-arg) rats. Arterial blood pressure, water intake, urine volume, and sodium excretion were measured. The 2K1C rats exhibited an increase in the mean arterial pressure (MAP) (from 106 ± 3 to 183 ± 5.8 mmHg, P < 0.01), whereas L-arg treatment induced a reduction in the MAP (143 ± 3.4 mmHg) without lowering it to the control level. Renal nerve denervation reduced the MAP to normotensive levels in 2K1C rats with or without chronic L-arg treatment. L-arg and denervation induced increases in water intake and urine volume, and L-arg caused a significant natriuretic effect. Our results suggest that renal sympathetic activity participates in the genesis and the maintenance of the hypertension and also demonstrate that treatment with L-arg alone is incapable of normalizing the MAP and that the effect of such treatment is not additive with the effect of kidney denervation.

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Section: Discussionmentioning

confidence: 99%

Role of Renal Nerves in the Treatment of Renovascular Hypertensive Rats withL-Arginine

Gouvêa

Tiradentes

Santuzzi

et al. 2014

International Journal of Hypertension

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“…Urinary sodium content was determined by flame photometry (mod. 943; Instrumental Laboratories, São Paulo, Brazil) and expressed as mEq/day [24].…”

Section: Methodsmentioning

confidence: 99%

Raloxifene Reduces Blood Pressure in Hypertensive Animals after Ovarian Hormone Deprivation

Moraes

Gouvêa

Gonçalves

et al. 2011

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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Raloxifene is a selective oestrogen receptor modulator that has been approved for the prevention and treatment of osteoporosis in post-menopausal women. Studies have revealed several effects of raloxifene on the cardiovascular system, which might contribute to the blood pressure regulatory mechanisms, particularly in the systemic arterial hypertension. Therefore, the aim of this study was to investigate the effects of raloxifene on the blood pressure, renal excretion of water and Na + and plasma nitrite ⁄ nitrate levels in 2-kidney-1-clip (2K1C) hypertensive female rats. The groups were as follows: hypertensive (2K1C), hypertensive ovariectomized (2K1C + OVX) and hypertensive ovariectomized treated with raloxifene (2K1C + OVX + R). Seven days after the surgery that produced menopause, 2K1C hypertension was produced in anaesthetized animals. Seven days after the clip application, the rats were put into metabolic cages to allow for the measurement of water ingestion and diuresis, and raloxifene was administered (2 mg ⁄ kg ⁄ day i.p., for 7 more days). We found a large reduction (p < 0.01) in mean arterial pressure (197 € 6 to 164 € 2 mmHg), an increase in renal excretion of sodium and water (p < 0.05) and an increase in plasma levels of nitrite ⁄ nitrate in 2K1C + OVX + R animals, when compared with the 2K1C (23.4 € 1 versus 14 € 0.5 nmol ⁄ mL; p < 0.01, respectively). These findings suggest that raloxifene exerted its antihypertensive effect, at least in part, by improving the renal excretion of sodium and water.In addition to its known effects on the reproductive system, nervous system and kidney [1][2][3][4], oestrogen exerts haemodynamic, metabolic and vascular effects that can explain the cardioprotection [5] seen in pre-menopausal women and in women who receive oestrogen replacement therapy for the relief of post-menopausal symptoms [6].Hormone replacement therapy (HRT) with oestrogen (alone or combined with a progestin) is usually prescribed for the relief of post-menopausal symptoms. In contrast to the increased risk of developing endometrial cancer [7], epidemiological data indicate that the use of oestrogen in women after menopause is associated with up to a 50% reduction in the incidence of cardiovascular diseases [8].The 2-kidney-1-clip (2K1C) hypertension model in rodents and stenosis of the renal artery in humans share pathophysiological mechanisms because they both primarily stimulate the renin-angiotensin system (RAS) [9,10], suggesting that the 2K1C model is relevant to clinical studies of hypertension. It is known that several humoral factors, including gonadal hormones, affect blood pressure in hypertensive patients [8]. For example, selective oestrogen receptor modulators (SERMs) such as raloxifene have several pharmacological effects on steroid hormone receptors, including both agonist and antagonist actions. Whether a SERM acts as an agonist or an antagonist depends on both the expression and spatial conformation of the a-oestrogen receptor (ER) and b-ER [11]. In addition, the local...

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“…16,20 In animal models of obstructive sleep apnea, RNA attenuated postapneic BP elevations in pigs and increased water excretion in rats. 80,84 RNA was evaluated recently in 10 patients with obstructive sleep apnea and resistant hypertension in a small, uncontrolled study. 47 BP results have been discussed above.…”

Section: Obstructive Sleep Apneamentioning

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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Influence of renal denervation on blood pressure, sodium and water excretion in acute total obstructive apnea in rats

Cited by 10 publications

References 39 publications

Role of Renal Nerves in the Treatment of Renovascular Hypertensive Rats withL-Arginine

Role of Renal Nerves in the Treatment of Renovascular Hypertensive Rats withL-Arginine

Raloxifene Reduces Blood Pressure in Hypertensive Animals after Ovarian Hormone Deprivation

Renal Nerve Ablation for Resistant Hypertension

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