The aim of our observation was to establish whether or not renal
sympathetic denervation (RSD) may help control blood pressure (BP) levels in patients with severe hypertension refractory to pharmacological therapy.
Out of a group of 12 patients, candidates for RSD, with uncontrolled hypertension and a systolic BP over 190 mm Hg on repeated measurements despite optimal medication, four patients were excluded for multiple renal
arteries and one for hyperaldosteronism. Seven patients had RSD using a Symplicity device (5M, 2F) with a mean age of 64.9 years. While all were followed up for a minimum of 6 months, follow-up duration in the majority of them was substantially longer (12-20 months). At six months post-RSD, six of the seven patients showed a decrease in systolic BP by at least 15 mm Hg
while receiving the same or fewer doses of antihypertensive agents. A similar response was seen in diastolic BP. The BP decrease was maintained throughout whole follow-up. In a small group of patients with severe hypertension, we demonstrated that renal sympathetic denervation is capable of reducing blood pressure even in patients with severe hypertension.
Renin-angiotensin system (RAS) plays a key role in the regulation of renal function, volume of extracellular fluid and blood pressure. The activation of RAS also induces oxidative stress, particularly superoxide anion (O2-) formation. Although the involvement of O2- production in the pathology of many diseases is known for long, recent studies also strongly suggest its physiological regulatory function of many organs including the kidney. However, a marked accumulation of O2- in the kidney alters normal regulation of renal function and thus may contribute to the development of salt-sensitivity and hypertension. In the kidney, O2- acts as vasoconstrictor and enhances tubular sodium reabsoption. Nitric oxide (NO), another important radical that exhibits opposite effects than O2-, is also involved in the regulation of kidney function. O2- rapidly interacts with NO and thus, when O2- production increases, it diminishes the bioavailability of NO leading to the impairment of organ function. As the activation of RAS, particularly the enhanced production of angiotensin II, can induce both O2- and NO generation, it has been suggested that physiological interactions of RAS, NO and O2- provide a coordinated regulation of kidney function. The imbalance of these interactions is critically linked to the pathophysiology of salt-sensitivity and hypertension., L. Kopkan, L. Červenka., and Obsahuje seznam literatury
The influence of renal nerves on the effects of concurrent NO synthase inhibition (10 mg kg-1 b.w. i.v. L-NAME) and ETA/ETB receptor inhibition (10 mg kg-1 b.w. i.v. bosentan) on renal excretory function and blood pressure in conscious spontaneously hypertensive rats (SHR) was investigated. L-NAME increased blood pressure, urine flow rate, fractional excretion of sodium, chloride and phosphate in both normotensive Wistar rats and SHR with intact renal nerves (p<0.01). GFR or RBF did not change in any of the groups investigated. The effects of L-NAME on renal excretory function were markedly reduced by bosentan and the values returned to control level in the normotensive rats, while in SHR the values were reduced by bosentan, but they remained significantly elevated as compared to control level (p<0.05). The hypertensive response induced by L-NAME in SHR is partially due to activation of endogenous endothelins, but it does not depend on renal nerves. Chronic bilateral renal denervation abolished the effect of L-NAME on sodium and chloride excretion in normotensive rats, whereas it did not alter this effect in SHR. The participation of endogenous endothelins in changes of renal excretory function following NO synthase inhibition is diminished in SHR as compared to Wistar rats., R. Girchev, P. Markova., and Obsahuje bibliografii a bibliografické odkazy
Varied causative and risk factors can lead to cardiac dysfunction. Cardiac dysfunction often evolves into heart failure by cardiac remodeling due to autonomic nervous system disturbance and neurohumoral abnormalities, even if the detriment factors are removed. Renal sympathetic nerve activity plays a pivotal regulatory role in neurohumoral mechanisms. The present study was designed to determine the therapeutic eff ects of renal sympathetic denervation (RSD) on cardiac dysfunction, fibrosis, and neurohumoral response in transverse aortic constriction (TAC) rats with chronic pressure overload. The present study demonstrated that RSD attenuated myocardial fibrosis and hypertrophy, and structural remodeling of the left atrium and ventricle, up -regulated cardiac β adrenoceptor (β -AR, including β 1 AR and β 2 AR) and sarco -endoplasmic reticulum Ca 2+ -ATP ase (SERCA) while down -regulated angiotensin II type 1 receptor (AT 1 R), and decreased plasma B -type natriuretic peptide (BNP), norepinephrine (NE) , angiotensin II (Ang II), and arginine vasopressin (AVP) levels in TAC rats with chronic pressure overload. We conclude that RSD attenuates myocardial fibrosis, the left atrial enlargement, and the left ventricular wall hypertrophy; inhibits the overdrive of the sympathetic ner vous system (SNS), renin- angiotensin -aldosterone system (RAAS), and AVP system in TAC rats with chronic pressure overload . RSD could be a promising non -pharmacological approach to control the progression of cardiac dysfunction., Z.-Z. Li, H. Jiang, D. Chen, Q. Liu, J. Geng, J.-Q. Guo, R.-H. Sun, G.-Q. Zhu, Q.-J. Shan., and Obsahuje bibliografii
The present paper is an extension to our earlier publication
(Šochman et al. 2016) documenting a beneficial effect of renal
sympathetic denervation on pharmacologically uncontrollable
hypertension in a group of seven patients followed up for
1-2 years post-procedure. The same patients remained on
ambulatory follow-up for another 5-6 years, with the beneficial
effect persisting throughout the follow-up period while on the
same medication.
Renální denervace je novou metodou v terapii farmakorezistentní hypertenze, která spočívá v selektivním přerušení sympatických vláken v adventicii renálních tepen. Dosud nebyly publikovány výsledky randomizovaných zaslepených studií, které by prokázaly efektivitu tohoto zákroku. Budoucnost ukáže, jestli bude metoda široce indikována v léčbě hypertenze či jiných chorob, které souvisejí se zvýšenou aktivitou sympatiku, nebo najde uplatnění pouze u selektovaných skupin pacientů nebo se stane slepou cestou lidského poznání., Renal denervation is a novel method in the treatment of resistant hypertension, which is based on selective ablation of sympathetic nervous fibres in the adventitia of renal arteries. The results of randomized, double‑blind trials which would prove efficacy of this method have not been published yet. We will find out in the near future whether this method will be widely indicated for the treatment of hypertension and other diseases associated with increased sympathetic activity, whether renal denervation will be applied only to selected groups of patients, or whether it is a wrong way on the road of human knowledge., and Mikušová T., Stárek Z., Jež J., Lehar F., Špinarová L.
Je jen mále oblastí ve vnitřním lékařství, které zaznamenaly extrémně rychlý rozmach a implementaci do klinické praxe v posledních 5 letech, jako je katetrizační renální denervace (RDN) u pacientů nejen s rezistentní hypertenzí. Základním problémem, který nebyl dostatečně řešen ve všech studiích s RDN, je skutečnost, že více než 50 % pacientů s tzv. rezistentní hypertenzí jsou ve skutečnosti nemocní neukáznění a neadherující k zavedené mediaci. Výsledky studie SYMPLICITY HTN-3 neprokázaly žádné rozdíly mezi změnou krevního tlaku u pacientů s provedenou RDN proti skupině s tzv. falešnou procedurou, tedy pokračující medikamentózní terapií. Budoucnost RDN je více než otazná a je potřeba vrátit se zpět k animálním studiím, které ověří reálnou efektivitu RDN redefinovat populaci pacientů indikovaných k RDN a ověřit použitelnost nově vyvinutých technologií., Transcatheter renal denervation (RDN) has been markedly applied and developed in clinical practice in past five years and not only for patients with resistant hypertension. The issue that more than 50% patients with so-called resistant hypertension are in fact patients without adherence to this type of mediation has not been resolved in RDN trials till now. The study Symplicity HTN-3 showed no differences in blood pressure change between the patients with RDN and group of patients after false procedure who continued in their drug therapy. Future of RDN is more than questionable and there is a need to return to animal studies that will verify the real effectiveness of RDN, subsequently, will redefine population of patients indicated for RDN and confirm the applicability of newly developed techniques., and Miloš Táborský, Marcela Schejbalová