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Resistant hypertension (RH) affects 10% to 18% of all patients with hypertension. It is diagnosed when blood pressure cannot be normalized despite the use of 3 classes of antihypertensive drugs (ACE inhibitors or sartans), calcium antagonists and diuretics in maximum doses. If the above-mentioned drugs are ineffective, spironolactone is most often administered. Recently, valsartan/sacubitrol and flozins have been increasingly used in resistant hypertension, which have been introduced for the treatment of diseases other than hypertension but can be a supplement to previously used drugs in resistant hypertension. Pharmaceutical companies are currently working on a dozen or so antihypertensive drugs. The most advanced studies concern aldosterone synthesis inhibitors, an endothelin receptor antagonist, and a drug that inhibits angiotensinogen synthesis. The results to date allow for the consideration of aprocitentan (a drug that inhibits endothelin receptors) or baxdrostat or another new aldosterone synthesis inhibitor in the treatment of resistant hypertension that does not respond to 4 drugs, including spironolactone. Further studies are needed to confirm the efficacy and safety of these new drugs in the treatment of resistant hypertension.

Structural and mechanical properties of the arterial wall are altered in patients with renal failure. Age and hypertension are known to affect the vessel wall structure. Aging process of arterial wall appears to be accelerated in patients with end-stage renal failure. The mechanisms responsible for reduced arterial compliance and distensibility in dialyse patients and renal transplant recipients without hypertension remain to be evaluated. 20 normotensive dialyse patients (D), 20 normotensive renal transplant recipients (T) and 20 healthy volunteers (N) matched for age, sex and blood pressure as controls were enrolled in to the study. Patients with cardiovascular risk factors and diabetes were excluded. The arterial blood pressure of all patients placed below 140/90 mmHg. The dialyse patients and renal transplant recipients were eligible for the study if the serum creatinine level was below 2 mg/dl. In all subjects, fasting concentrations of serum creatinine, total cholesterol, HDL-cholesterol, LDL-cholesterol, hemoglobin and glucose were determined at enrollment to the study. Long-term immunosuppression consisted of cyclosporine and prednisolone. Blood pressure was measured using an automatic sphygmomanometer (Criticon Dinamap model 1846 SX). Pulse wave velocity (PWV) was evaluated using non-invasive automatic Complior device. The vessel wall properties of the left common carotid artery were studied using multigate pulsed Doppler's system (Pie Medical Equipment BV Maastricht, The Netherlands). The frequency of transducer used was 7.5 MHz. With this non-invasive method, the end-diastolic diameter (d) and the systolic increase of vessel diameter (distension delta d) were measured using ECG trigger. From these data relative systolic increase of vessel diameter (delta d/d) and arterial wall distensibility coefficient (DC) were calculated. Simultaneously with the ultrasound measurements at the left common carotid artery carotid pulse waveforms are recorded using applanation tonometry (Micro Tip Pulse Transducer, SPT 301 and Transducer Control Unit TCB-500, Millar Instruments, Houston, TX, USA). Systolic blood pressure (SBP) and central pulse pressure (CPP) were significantly higher in (T) than in (D) and (N) group respectively 139 +/- 18 mmHg and 58 +/- 16 mmHg vs 127 +/- 13 mmHg and 49 +/- 11 mmHg and 132 mmHg and 50 +/- 11 mmHg. The end-diastolic diameter (d) did not change significantly between all groups. The systolic increase of vessel diameter (distension delta d) was significantly lower in patients group (D) and (T) respectively 461 +/- 33 microm and 501 +/- 34 microm than in controls. Similar relative systolic increase of vessel diameter (delta d/d) was in these groups significantly lower than in healthy volunteers, respectively (D) 6.26 +/- 0.5%, (T) 6.91 +/- 0.4% vs (N) 9.14 +/- 0.4%. The distensibility coefficient were also significantly lower in (D) and (T) than in (N) groups respectively (D) 18.31 +/- 1.4 10(-3)/kPa and (T) 17.97 +/- 1.4 10(-3)/kPa and (N) 24.3 +/- 0.5 10(-3)/kPa. PWV in both groups of patients was statistically significant higher than in control group correspondingly (D) 11.2 +/- 1.02 m/s and (T) 12.8 +/- 1.12 m/s, (N) 9.5 +/- 0.88 m/s. There was significant correlation between the change of arterial DC, PWV and CPP in (T) group (n = 20; r = -0.42; p < 0.01 and n = 20; r = 0.47; p < 0.05). The arterial wall elastic properties in dialyse and renal recipients patients are decreased. End-stage renal disease accelerates arterial stiffening despite arteriosclerosis and hypertension. Renal transplantation do not reverse lost of elastic properties of arteries in end-stage renal insufficiency.

Lack of normalization of arterial pressure in spite of treatment of hypertension is most frequently caused by irregular and incomplete taking of hypotensive drugs or by erroneous medical instructions (drug interactions). "True" resistance to 3 simultaneously administered hypotensive drugs in optimal doses may be caused by secondary hypertension. In a part of cases of refractory essential hypertension an increased insulin concentration is found. In the paper the importance is discussed of "resistance" to insulin in the development of hypertension.