scholarly journals Mechanisms for the Development of Blood Pressure Variability and the Potential of Antihypertensive Drugs in Their Correction

Kardiologiia ◽  
2019 ◽  
Vol 59 (11) ◽  
pp. 56-65 ◽  
Author(s):  
A. I. Kochetkov ◽  
O. D. Ostroumova ◽  
E. V. Borisova ◽  
G. F. Piksina

Blood pressure variability (BPV) is the fluctuations of blood pressure over a certain period of time under the influence of various factors. The issue of increased BPV is of particular clinical importance due to high predictive value of this parameter as a risk factor for fatal and non-fatal cardiovascular, cerebrovascular and renal events. It is proved that in the BPV increasing, the key role is played by impairments in arterial baroreflexes, which, in turn, are mediated by increased vascular stiffness, impact of angiotensin II and the sympathetic nervous system, endothelial dysfunction, nitric oxide deficiency and aging, including the vascular aging. Antihypertensive drugs that targeting largest amount of pathophysiological mechanisms in BPV increasing have a most advantages in correcting excessive pressure fluctuations. In this regard such drugs are perindopril and amlodipine, which can eliminate almost the entire spectrum of increased BPV causes and, therefore, optimally reduce the cardiovascular risk.

2001 ◽  
Vol 20 (2) ◽  
pp. 17-24 ◽  
Author(s):  
S.C. Malpas ◽  
B.L. Leonard ◽  
S.-J. Guild ◽  
J.V. Ringwood ◽  
M. Navakatikyan ◽  
...  

2020 ◽  
Vol 92 (4) ◽  
pp. 91-97
Author(s):  
A. S. Tokareva ◽  
N. Yu. Borovkova

A present review is devoted to the current state of the problem of blood pressure variability (BPV) in hemodialysis patients. The BPV classification and clinical significance of BPV metrics are discussed. The results of cohort and randomized studies on the high BPV influence on outcomes in hemodialysis patients, as well as on the possibilities of antihypertensive drugs in the treatment of high BPV in dialysis patients, are presented.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Laure Rouch ◽  
Philipe de Souto Barreto ◽  
Olivier Hanon ◽  
Jacques Amar ◽  
Yves Rolland ◽  
...  

Introduction: Visit-to-visit blood pressure variability (BPV) has been associated with greater cardiovascular and all-cause mortality, cognitive impairment, and incident dementia. It may also represent a decline in homeostatic mechanisms in blood pressure (BP) regulation associated with frailty, one of the most problematic expression of population aging. Hypothesis: We hypothesized that visit-to-visit systolic (SBPV), diastolic (DBPV), mean arterial (MAPV) and pulse pressure (PPV) variability are associated with greater incident frailty. Methods: We included 1,394 non-frail community-dwelling participants aged ≥ 70 years from the Multidomain Alzheimer Preventive Trial (MAPT) who underwent repeated clinical examinations over a 5-year follow-up period. SBPV, DBPV, MAPV and PPV were evaluated using standard deviation, coefficient of variation (CV), average real variability, successive variation, variation independent of mean and residual standard deviation. Incident frailty was assessed using the Fried phenotype. Cox proportional hazards models were used for the analyses. Results: Higher SBPV was significantly associated with increased risk of incident frailty (1-sd increase of CV: HR = 1.18, 95% CI [1.02-1.37], p=0.03) after adjustment for demographics, body mass index, stroke, ischemic heart disease, diabetes, heart failure, antihypertensive drugs, systolic BP, MAPT intervention groups and baseline pre-frail status. Similar results were observed with all indicators of variability. DBPV and MAPV were not associated with incident frailty (p=0.6 and p=0.2, respectively). Interestingly, higher PPV was also associated with a greater risk of developing frailty over time (1-sd increase of CV: HR = 1.17, 95% CI [1.01-1.35], p=0.03). Conclusion: Independently of BP, higher SBPV and PPV are major clinical predictors of incident frailty. Our findings support the concept of BP physiological dysregulation underlying the frail state and suggest that controlling BP instability could be a promising interventional target in preventing frailty.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Bruno Igreja ◽  
Nuno M Pires ◽  
Lyndon C Wright ◽  
Patrío Soares-da-Silva

The sympathetic nervous system can alter blood pressure by modulation of cardiac output, peripheral vascular resistance and renal function. One strategy for controlling sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH; EC 1.14.17.1 ), the enzyme that catalyses the conversion of dopamine (DA) to NE in sympathetic nerves. BIA 5-1058 is a reversible DβH inhibitor that decreases NE levels in peripheral sympathetically innervated tissues slowing down sympathetic nervous system drive, without effect in brain tissues. In freely moving SHR implanted with radio-telemetry transmitters single administration of BIA 5-1058 showed a dose (3, 30 and 100 mg/Kg) and time dependent effect on blood pressure with no significant effect on heart rate (HR) and total activity monitored over a 96-hour period. The maximum reduction on systolic blood pressure (SBP) was -10.8, -21.1 and -35.2 mmHg for 3, 30 and 100 mg/Kg, respectively and the maximum reduction on diastolic blood pressure (DBP) was -9.9, -18.4 and -24.8 mmHg for 3, 30 and 100 mg/Kg, respectively. The antihypertensive effect of BIA 5-1058 (30 mg/Kg) was further evaluated in combination with efficacious doses of well-known antihypertensive drugs, like the ACE inhibitor captopril, the AT1 receptor antagonist losartan, the diuretic hydrochlorothiazide, beta-blocker metoprolol, the alpha-1 receptor antagonist prazosin, and the calcium channel blocker diltiazem. All drugs were administered orally (single dose) in a cross-over design and the effect was monitored for 72 hours. The combination of BIA 5-1058 with any of the tested antihypertensive drugs caused a stronger and prolonged blood pressure decrease than any of the compounds alone.In conclusion, peripheral DβH inhibitors can be used, alone or in combination with others antihypertensive drugs, to reduce blood pressure.


2007 ◽  
Vol 156 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Félix Vargas ◽  
Juan Manuel Moreno ◽  
Rosemary Wangensteen ◽  
Isabel Rodríguez-Gómez ◽  
Joaquín García-Estañ

The experimental model of chronic inhibition of nitric oxide (NO) production has proven to be a useful tool to study cardiovascular and renal lesions produced by this type of hypertension, which are similar to those found in human hypertension. It also offers a unique opportunity to study the interaction of NO with the humoral systems, known to have a role in the normal physiology of vascular tone and renal function. This review provides a thorough and updated analysis of the interactions of NO with the endocrine system. There is special focus on the main vasoactive factors, including the renin-angiotensin-aldosterone system, catecholamines, vasopressin, and endothelin among others. Recent discoveries of crosstalk between the endocrine system and NO are also reported. Study of these humoral interactions indicates that NO is a molecule with ubiquitous function and that its inhibition alters virtually to all other known regulatory systems. Thus, hypothyroidism attenuates the pressor effect of NO inhibitor N-nitro-L-arginine methyl ester, whereas hyperthyroidism aggravates the effects of NO synthesis inhibition; the sex hormone environment determines the blood pressure response to NO blockade; NO may play a homeostatic role against the prohypertensive effects of mineralocorticoids, thyroid hormones and insulin; and finally, NO deficiency affects not only blood pressure but also glucose and lipid homeostasis, mimicking the human metabolic syndrome X, suggesting that NO deficiency may be a link between metabolic and cardiovascular disease.


2008 ◽  
Vol 294 (2) ◽  
pp. F362-F370 ◽  
Author(s):  
Mattias Carlström ◽  
Russell D. Brown ◽  
Jenny Edlund ◽  
Johan Sällström ◽  
Erik Larsson ◽  
...  

Hydronephrotic animals develop renal injury and hypertension, which is associated with an abnormal tubuloglomerular feedback (TGF). The TGF sensitivity is coupled to nitric oxide (NO) in the macula densa. The involvement of reduced NO availability in the development of hypertension in hydronephrosis was investigated. Hydronephrosis was induced by ureteral obstruction in young rats. Blood pressure and renal excretion were measured in adulthood, under different sodium conditions, and before and after chronic administration of either NG-nitro-l-arginine methyl ester (l-NAME) or l-arginine. Blood samples for ADMA, SDMA, and l-arginine analysis were taken and the renal tissue was used for histology and determination of NO synthase (NOS) proteins. TGF characteristics were determined by stop-flow pressure technique before and after administration of 7-nitroindazole (7-NI) or l-arginine. Hydronephrotic animals developed salt-sensitive hypertension, which was associated with pressure natriuresis and diuresis. The blood pressure response to l-NAME was attenuated and l-arginine supplementation decreased blood pressure in hydronephrotic animals, but not in the controls. Under control conditions, reactivity and sensitivity of the TGF response were greater in the hydronephrotic group. 7-NI administration increased TGF reactivity and sensitivity in control animals, whereas, in hydronephrotic animals, neuronal NOS (nNOS) inhibition had no effect. l-Arginine attenuated TGF response more in hydronephrotic kidneys than in controls. The hydronephrotic animals displayed various degrees of histopathological changes. ADMA and SDMA levels were higher and the renal expressions of nNOS and endothelial NOS proteins were lower in animals with hydronephrosis. Reduced NO availability in the diseased kidney in hydronephrosis, and subsequent resetting of the TGF mechanism, plays an important role in the development of hypertension.


2014 ◽  
Vol 155 (42) ◽  
pp. 1661-1672
Author(s):  
Ede Kékes ◽  
István Kiss

Authors have collected and analyzed literature data on blood pressure variability. They present the methods of blood pressure variability measurement, clinical value and relationships with target organ damages and risk of presence of cardiovascular events. They collect data about the prognostic value of blood pressure variability and the effects of different antihypertensive drugs on blood pressure variability. They underline that in addition to reduction of blood pressure to target value, it is essential to influence blood pressure fluctuation and decrease blood pressure variability, because blood pressure fluctuation presents a major threat for the hypertensive subjects. Data from national studies are also presented. They welcome that measurement of blood pressure variability has been included in international guidelines. Orv. Hetil., 2014, 155(42), 1661–1672.


1970 ◽  
Vol 6 (2) ◽  
pp. 93-96
Author(s):  
Uzzal Kanti Das ◽  
Syed Ali Ahsan ◽  
Mohammad Salman ◽  
Mohammad Ferdous Ur Rahaman ◽  
Md Mizanur Rahman Khan ◽  
...  

Nebivolol is a vasodilating β-blocker, which can be distinguished from other β-blockers by its haemodynamic profile. It combines β-adrenergic blocking activity with a vasodilating effect mediated by the endothelial Larginine nitric oxide (NO) pathway. The blood pressure lowering effect of nebivolol is linked to a reduction in peripheral resistance and an increase in stroke volume and preservation of cardiac output. Clinical trials have demonstrated that nebivolol reduces blood pressure similarly to atenolol, bisoprolol, amlodipine, nifedipine, lisinopril, and hydrochlorothiazide. The tolerability of nebivolol is similar to or better than that of these agents. In general, response rates to treatment are higher and the frequency and severity of adverse events are either comparable or lower with nebivolol. Endothelium-derived NO is important in the regulation of large arterial stiffness, which in turn is a major risk factor for cardiovascular disease. Therefore, antihypertensive drugs, such as nebivolol, that also improve endothelial function and decrease arterial stiffness, may contribute to a reduction in cardiovascular risk.Key words: Vasodilating β-blocker; nitric oxide (NO); peripheral resistance; arterial stiffness DOI: 10.3329/uhj.v6i2.7254University Heart Journal Vol. 6, No. 2, July 2010 pp.93-96


1996 ◽  
Vol 57 (3) ◽  
pp. 181-183 ◽  
Author(s):  
Benno Nafz ◽  
Armin Just ◽  
Harald M. Stauβ ◽  
Claus D. Wagner ◽  
Heimo Ehmke ◽  
...  

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