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Baroreceptor activation therapy (BAT) has been available for several years for treatment of therapy-refractory hypertension (trHTN). This procedure is currently being carried out in a limited number of centers in Germany, also with the aim of offering a high level of expertise through sufficient experience; however, a growing number of patients who are treated with BAT experience problems that treating physicians are confronted with in routine medical practice. In order to address these problems, a consensus conference was held with experts in the field of trHTN in November 2016, which summarizes the current evidence and experience as well as the problem areas in handling BAT patients.

This commentary summarizes the expert consensus and recommendations of the working group 'Herz und Niere' of the German Society of Cardiology (DGK), the German Society of Nephrology (DGfN) and the German Hypertension League (DHL) on renal denervation for antihypertensive treatment. Renal denervation is a new, interventional approach to selectively denervate renal afferent and efferent sympathetic fibers. Renal denervation has been demonstrated to reduce office systolic and diastolic blood pressure in patients with resistant hypertension, defined as systolic office blood pressure ≥ 160 mm Hg and ≥ 150 mm Hg in patients with diabetes type 2, which should currently be used as blood pressure thresholds for undergoing the procedure. Exclusion of secondary hypertension causes and optimized antihypertensive drug treatment is mandatory in every patient with resistant hypertension. In order to exclude pseudoresistance, 24-hour blood pressure measurements should be performed. Preserved renal function was an inclusion criterion in the Symplicity studies, therefore, renal denervation should be only considered in patients with a glomerular filtration rate 45 ml/min. Adequate centre qualification in both, treatment of hypertension and interventional expertise are essential to ensure correct patient selection and procedural safety. Long-term follow-up after renal denervation and participation in the German Renal Denervation (GREAT) Registry are recommended to assess safety and efficacy after renal denervation over time.

To compare the effects of two long-acting calcium antagonists of different types on cardiovascular stress responses in hypertension.One-hundred and forty-five patients with mild to moderate hypertension and a mean (+/- s.e.mean) age of 51 +/- 0.9 years received for 8 weeks the phenylalkylamine verapamil sustained release (240 mg) and the dihydropyridine amlodipine (5 mg) in a double-blind cross-over design, both after 4 weeks of placebo. Blood pressure, heart rate and plasma noradrenaline were monitored during 3 min of sustained isometric handgrip and 2 min of cold pressor.Blood pressure was equally reduced by both drugs. After 3 min handgrip, systolic blood pressure, heart rate and rate-pressure product were lower with verapamil compared with amlodipine. Verapamil attenuated the increases in systolic blood pressure (25 +/- 2 vs 30 +/- 2 mmHg, difference 4.6, 95% CI (1.0, 8.1), P0.01) and rate-pressure product (3.1 +/- 0.2 vs 3.6 +/- 0.3 x 10(3) mmHg x beats min(-1), difference 0.5, 95% CI (0.1, 0.9), P0.01) during handgrip compared with amlodipine. Similar results were observed during cold pressor. Plasma noradrenaline levels were lower with verapamil compared with amlodipine at rest and after both tests, but the increases in plasma noradrenaline were not significantly different.Verapamil is more effective in reducing blood pressure and rate-pressure product responses to stress compared with amlodipine. Although plasma noradrenaline is lower with verapamil at rest and after stress, the increase during stress is not different.

There is evidence that secondary hyperparathyroidism alters arterial vessel wall properties. However, it is unclear whether effects of parathyroid hormone (PTH) on the vascular wall are direct or permissive and related to hypertension and renal failure. To assess early direct effects of PTH on large artery wall properties isobaric distensibility (DC), pulse wave velocity (PWV) and intima-media thickness (IMT) were studied before and after parathyroidectomy (Ptx) in patients with primary hyperparathyroidism (pHPT).DC and IMT of the brachial and carotid artery were measured by echo-tracking and tonometry, PWV by the automatic Complior-device at baseline and 6 months after Ptx in 20 patients with pHPT (data mean +/- SEM, age 45+/-5 years, PTH 240+/-61 ng/l). Cardiovascular risk factors like diabetes, hypertension, renal insufficiency and hypercholesterolemia were excluded. Twenty healthy volunteers matched for age, sex and blood pressure served as controls.Six months after Ptx, PTH decreased to normal; however, blood pressure levels and vessel wall parameter remained unchanged. At baseline, there were no significant differences in brachial and carotid IMT (0.48+/-0.04 and 0.62+/-0.04 mm vs. 0.47+/-0.06 and 0.61+/-0.06 mm), radial and aortic PWV (9.1+/-0.4 and 9.9+/-0.7 m/s vs. 9.2+/-0.5 and 10.0+/-0.6 m/s), brachial and isobaric carotid DC (10.1+/-1.4 and 19.5+/-3.4 10(-3)/kPa vs. 9.1+/-0.9 and 20.4+/-3.2 10(-3)/kPa) or artery diameter between patients and controls.Structural and viscoelastic properties of large arteries are not disturbed and not influenced by parathyroidectomy in patients with early pHPT devoid of hypertension and renal disease. We conclude that increased PTH levels per se are not associated with alterations of mechanical arteriall wall properties; permissive factors like renal insufficiency may be necessary to mediate vessel wall alterations in patients with hyperparathyroidism.

There are now numerous studies demonstrating that essential hypertension is accompanied by sympathetic activation. Using drugs which block cardiac sympathetic effects, it could be shown that a noticeable fraction of subjects with borderline hypertension had an increased sympathetic drive. A meta-analysis of studies on plasma noradrenaline levels as an indirect marker of sympathetic tone reported that noradrenaline concentrations were significantly elevated in patients with essential hypertension as compared with normotensive control subjects. In addition, it could be shown that the rate of noradrenaline spillover from sympathetic nerve terminals was sometimes increased in essential hypertension, particularly in young hypertensive subjects. Additional data have emerged by direct measurement of sympathetic nerve traffic to skeletal muscle circulation using a microelectrode technique. Most studies using this method have demonstrated increased sympathetic nerve activity in patients with essential hypertension. In contrast, patients with secondary hypertension did not differ from normotensive subjects. Taken together, the data available at present show that sympathetic activation is a specific feature of essential hypertension and that it may play a pathogenetic role in this disease.

The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS).In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P.05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P.05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P.05).Acute short-term passive (sidestream) smoke exposure elicits a modest increase in MSNA in healthy non-smokers but does not change HR, BP, or FVR.