scholarly journals Hormonal Mechanisms in Essential Hypertension

2021 ◽  
Vol 18 (3) ◽  
pp. 57-68
Author(s):  
Mariana Dobrescu ◽  
Diana Păun ◽  
Sorina Buculei ◽  
Daniel Grigorie ◽  
Cătălina Poiană

Abstract “Essential” hypertension is related to multiple mechanisms that affect cardiac output and peripheral resistance and is a consequence of the interaction between external factors and genetic factors. Neuro-hormonal factors are essential in the pathophysiology of hypertension and among them the renin-angiotensin-aldosterone system (RAAS) has a main role in the physiological and pathological response of the cardiovascular system. RAAS functions as an endocrine system, but also has paracrine and autocrine functions in many tissues and organs. RAAS regulates extracellular fluid volume and peripheral resistance via systemic and local actions in various tissues. RAAS also participates in endothelial dysfunction, inflammation and vascular fibrosis, cardiac fibrosis and cardiovascular remodelling, with worsening hypertension and target organ injury. Aldosterone is involved in “essential” hypertension via discrete variations in the regulation of aldosterone synthesis in the absence of confirmed primary hyperaldosteronism. A complete evaluation of these systems is needed for a thorough understanding of hypertension.

2016 ◽  
Vol 310 (3) ◽  
pp. R217-R229 ◽  
Author(s):  
Roger G. Evans ◽  
Peter Bie

The “Guytonian paradigm” places the direct effect of arterial pressure, on renal excretion of salt and water, at the center of long-term control of blood pressure, and thus the pathogenesis of hypertension. It originated in the sixties and remains influential within the field of hypertension research. However, the concept of one central long-term feedback loop, through which arterial pressure is maintained by its influence on renal function, has been questioned. Furthermore, some concepts in the paradigm are undermined by experimental observations. For example, volume retention and increased cardiac output induced by high salt intake do not necessarily lead to increased arterial pressure. Indeed, in multiple models of salt-sensitive hypertension the major abnormality appears to be failure of the vasodilator response to increased cardiac output, seen in salt-resistant animals, rather than an increase in cardiac output itself. There is also evidence that renal control of extracellular fluid volume is driven chiefly by volume-dependent neurohumoral control mechanisms rather than through direct or indirect effects of changes in arterial pressure, compatible with the concept that renal sodium excretion is controlled by parallel actions of different feedback systems, including hormones, reflexes, and renal arterial pressure. Moreover, we still do not fully understand the sequence of events underlying the phenomenon of “whole body autoregulation.” Thus the events by which volume retention may develop to hypertension characterized by increased peripheral resistance remain enigmatic. Finally, by definition, animal models of hypertension are not “essential hypertension;” progress in our understanding of essential hypertension depends on new results on system functions in patients.


2021 ◽  
Vol 10 (10) ◽  
pp. 2075
Author(s):  
Weronika Wasyluk ◽  
Martyna Wasyluk ◽  
Agnieszka Zwolak

Sepsis is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. One of the elements of dysregulated host response is an endocrine system disorder. Changes in its functioning in the course of sepsis affect almost all hormonal axes. In sepsis, a function disturbance of the hypothalamic–pituitary–adrenal axis has been described, in the range of which the most important seems to be hypercortisolemia in the acute phase. Imbalance in the hypothalamic–pituitary–thyroid axis is also described. The most typical manifestation is a triiodothyronine concentration decrease and reverse triiodothyronine concentration increase. In the somatotropic axis, a change in the secretion pattern of growth hormone and peripheral resistance to this hormone has been described. In the hypothalamic–pituitary–gonadal axis, the reduction in testosterone concentration in men and the stress-induced “hypothalamic amenorrhea” in women have been described. Catecholamine and β-adrenergic stimulation disorders have also been reported. Disorders in the endocrine system are part of the “dysregulated host response to infection”. They may also affect other components of this dysregulated response, such as metabolism. Hormonal changes occurring in the course of sepsis require further research, not only in order to explore their potential significance in therapy, but also due to their promising prognostic value.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Yufeng Huang ◽  
Guangyu Zhou ◽  
Jie Wu ◽  
Chunyan Gu ◽  
Alfred Cheung

Plasma prorenin is commonly elevated in diabetic patients and appears to predict the development of diabetic nephropathy. However, the pathological role of prorenin is unclear. In this study, a transgenic, inducible, hepatic prorenin-overexpressing rat model was generated and the effect of prorenin in organ injury was examined. Four groups of rats (Cyp1a1 prorenin transgenic male and female rats and nontransgenic littermates) were assigned to receive a diet containing 0.3% of the transgene inducer indole-3-carbinol (I3C) for 4 weeks. Plasma prorenin concentration rose from 23±6 to 208±44 (μg/ml) and MAP increased from 77±5 to 138±17 (mmHg), whereas renal prorenin/renin protein expression was unchanged, in transgenic rats fed with I3C diet. The intact prorenin, not renin, in plasma and urine samples was further observed by western blot analysis. Importantly, transgenic rats with high levels of prorenin developed albuminuria, glomerular and tubulointerstitial fibrosis associated with increased expression of TGFß1, PAI-1, collagen and fibronectin. These rats also exhibited cardiac hypertrophy determined by echocardiography, with elevated ratio of heart weight to body weight. Cardiac collagen in interstitial and perivascular area was prominent, accompanied by the increases in mRNA contents of ANP, BNP, ß-MHC, TGFß1 and PAI-1 in the heart tissue. Furthermore, renal protein levels of phosphor-NF-kB-p65 and MCP-1, NAPDH oxidase and MDA, phospho-ß-catenin and phospho-Akt were dramatically increased in prorenin overexpressed rats. These results indicate that prorenin, without being converted to renin, causes arterial hypertension, renal and cardiac fibrosis independently via the induction of inflammation, oxidative stress and the ß-catenin and Akt-mediated signals.


2019 ◽  
Author(s):  
li anle ◽  
Qian Peng ◽  
Yue Qin Shao ◽  
Yi Ying Zhang ◽  
Fang Xiang

Abstract Importance Genetic factors are important influencing factors of essential hypertension, and family history (FH) is an important marker of genetic factors. Objective To explore the association between family history and the onset age of essential hypertension in Han population in Shanghai China. Methods According to l:l matched pairs design,342 precursor of hypertension and 342 controls were selected and investigate their nuclear family members in the case-control study. The diagnostic information of hypertension in all relatives of these two groups was investigated. The method of genetic epidemiology research was used to explore the effect of family history. Results The average prevalence of hypertension was 23.32%. The prevalence of hypertension of first-degree relatives was 33.99%; the prevalence of second- degree relatives was 17.60%; the prevalence of third-degree relatives was 13.51%. All prevalence of hypertension of case group relatives were significantly higher than that of control group relatives. The average onset age in population with positive FH is 48.74±11.16 years old, and the average onset age in population with negative FH is 54.38±9.87 years old. The difference about two FH groups showed statistically significant (t=4.589, P<0.001). The average onset age of offspring with father, mother, grandpa, grandma, maternal grandpa or maternal grandma positive was respectively 48.42± 11.16, 49.16±11.12, 39.55±11.95, 39.88±11.90, 43.67±9.77 or 43.64±10.21 years old; and the average onset age of children with father, mother, grandpa, grandma, maternal grandpa or maternal grandma negative was respectively 51.90± 10.81, 51.17±11.04, 51.07±10.59, 51.08±10.60, 50.50±11.09 or 50.57±11.06 years old. The difference about two groups showed statistically significant. Conclusion Family history has a positive effect on the occurrence of hypertension, and lead to earlier age of onset of offspring. The effects are different among parent and grandparent in Han in Shanghai China.


2019 ◽  
Vol 26 (1) ◽  
Author(s):  
Henry Sung-Ching Wong ◽  
Ying-Ju Lin ◽  
Hsing-Fang Lu ◽  
Wen-Ling Liao ◽  
Chien-Hsiun Chen ◽  
...  

Abstract Background Genetic factors, dysregulation in the endocrine system, cytokine and paracrine factors are implicated in the pathogenesis of familial short stature (FSS). Nowadays, the treatment choice for FSS is limited, with only recombinant human growth hormone (rhGH) being available. Methods Herein, starting from the identification of 122 genetic loci related to FSS, we adopted a genetic-driven drug discovery bioinformatics pipeline based on functional annotation to prioritize crucial biological FSS-related genes. These genes were suggested to be potential targets for therapeutics. Results We discovered five druggable subnetworks, which contained seven FSS-related genes and 17 druggable targerts. Conclusions This study provides a valuable drug repositioning accompanied by corresponding targetable gene clusters for FSS therapy.


1977 ◽  
Vol 52 (6) ◽  
pp. 591-597 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
T. Reybrouck ◽  
P. Lijnen ◽  
L. Billiet ◽  
...  

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = −0·45), indicating that ‘high-renin’ essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = −0·46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in ‘low-renin’ hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0·42). 5. Multiple regression analysis indicates that the described relationships were independent of age.


1972 ◽  
Vol 43 (2) ◽  
pp. 165-170 ◽  
Author(s):  
P. Sederberg-Olsen ◽  
H. Ibsen

1. In ten patients with essential hypertension treated with propranolol (320 mg daily for 4 months) plasma volume and extracellular fluid volume were determined. 2. A significant increase in extracellular fluid volume (ECFV) was found, but there was no significant change in plasma volume. 3. The genesis of the increase found in ECFV is briefly discussed.


1976 ◽  
Vol 51 (s3) ◽  
pp. 525s-526s
Author(s):  
H. Æ. Jensen ◽  
K. Rasmussen ◽  
N. Mosbæk

1. The β1-adrenoreceptor-blocking agent atenolol was studied in the treatment of twelve out-patients with essential hypertension. 2. With a mean dose of 110 mg of atenolol daily (range 75–200 mg/day) we observed a pronounced decrease in blood pressure. 3. Only minimal side effects were seen. 4. Cardiac output decreased from 4·6 to 3·4 l/min during treatment. This decrease did not correlate with the decrease in blood pressure but correlated well with the changes in calculated total peripheral resistance.


1978 ◽  
Vol 55 (s4) ◽  
pp. 69s-71s ◽  
Author(s):  
Y. Miura ◽  
K. Kobayashi ◽  
H. Sakuma ◽  
H. Tomioka ◽  
M. Adachi ◽  
...  

1. Plasma noradrenaline concentrations and haemodynamic status were simultaneously studied in young patients with uncomplicated essential hypertension and in age-matched normal controls. 2. Resting plasma noradrenaline in the controls tended to increase slightly, but progressively, with age. The hypertensive subjects had significantly higher plasma noradrenaline concentrations than those in the controls, but these values did not show any age-related variation. The response of plasma noradrenaline to the standing position tended to increase with age in the controls, whereas plasma noradrenaline in the hypertensive subjects showed a wide range of responses without any fixed relationship with age. 3. The cardiac index was significantly greater in the labile hypertensive subjects than in the controls, whereas total peripheral resistance was significantly greater in the sustained hypertensive subjects than in the labile patients and in the controls. Mean arterial pressure in these patients was closely related with the values of total peripheral resistance rather than with the cardiac index. 4. Of the patients with raised plasma noradrenaline 80% showed significantly increased values of either total peripheral resistance or cardiac index. Plasma noradrenaline was correlated significantly to total peripheral resistance, and marginally to mean arterial pressure. 5. These findings support the view that sympathetic nervous overactivity is an important factor underlying the haemodynamic findings in these patients.


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