scholarly journals Hormonal aspects in the pathogenesis of arterial hypertension in young obese patients in young obese patients

1993 ◽  
Vol 39 (5) ◽  
pp. 26-28
Author(s):  
I. V. Tereschenko ◽  
N. L. Vladimirskaya
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Arterial Hypertension ◽  
Blood Lipids ◽  
Plasma Renin ◽  
Obese Patients ◽  
Hormonal Dysfunction ◽  
Group 2 ◽  
Early Manifestation ◽  
Group 1

Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, 6-endorphine, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.

Differential Effects of Acute and Chronic β-Adrenoreceptor Blockade on Blood Pressure and the Renin—Angiotensin—Aldosterone System in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 537s-540s
Author(s):  
R. Kolloch ◽  
K. O. Stumpe ◽  
H. Vetter ◽  
W. Gramann ◽  
F. Krück
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Receptor Blockade ◽  
Plasma Aldosterone Concentration ◽  
Group 2 ◽  
Β Receptor ◽  
Group 1

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0·79) or chronic (r = 0·4) β-receptor blockade. 4. In group 1, after β-receptor blockade the day—night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced β-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the β-blocking drugs.

Time Course of Systemic and Renal Plasma Prostanoid Concentrations and Renal Function in Ovine Hyperdynamic Sepsis

1994 ◽  
Vol 86 (5) ◽  
pp. 599-610 ◽  
Author(s):  
Andreas Weber ◽  
Ian M. Schwieger ◽  
Olivier Poinsot ◽  
Denis R. Morel
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Creatinine Clearance ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
Endotoxin Infusion ◽  
Group 2 ◽  
Group 1

1. We continuously recorded systemic and renal haemodynamic changes, and arterial, renal venous and urinary concentrations of thromboxane B2, 6-keto-prostaglandin F1α and prostaglandin E2, and determined their relationship to renal function in an ovine model of progressive hyperdynamic sepsis. 2. Nine chronically instrumented unanaesthetized sheep were given a continuous intravenous infusion of Escherichia coli endotoxin (20 ng min−1 kg−1) for 3 days. 3. Within the first 12 h of infusion, endotoxin induced a major hypotensive septic syndrome, including a persistent 30% reduction in mean arterial pressure, a 50% decrease in systemic vascular resistance and a 50% increase in mean pulmonary artery pressure, associated with severe lactacidaemia. 4. Renal blood flow decreased by 40%, and creatinine clearance, urine flow, and fractional sodium excretion decreased by more than 75%, of baseline values. After 12 h of endotoxin infusion, cardiac output increased two-fold and renal blood flow recovered to baseline values, whereas creatinine clearance remained depressed. Four sheep died between 13 and 22 h of endotoxaemia; these animals (allocated to group 1) presented a significantly and persistently more reduced renal blood flow (−23%) and creatinine clearance (−77%) after 4 h than the remaining five sheep (allocated to group 2), which survived more than 36 h (−16% and −21%, respectively), whereas systemic and pulmonary haemodynamic and gas exchange data remained similar in both groups. 5. The more pronounced decreases in renal blood flow, creatinine clearance and urine flow in group 1 were associated with higher plasma renin activity and plasma 6-keto-prostaglandin F1α concentrations and a lower fractional urinary excretion of 6-keto-prostaglandin F1α than in group 2, whereas plasma thromboxane B2 concentrations were similarly increased in both groups. Plasma prostaglandin E2 concentrations and urinary excretion were not notably affected by endotoxin infusion in either group. 6. Our results are not in favour of a significant renal production of any of these three prostanoids during endotoxaemia. In both groups, values of creatinine clearance were linearly correlated with simultaneous mean arterial pressure values after starting endotoxin infusion (group 1: creatinine clearance = 1.99 × mean arterial pressure −105, r = 0.95; group 2: creatinine clearance = 2.06 × mean arterial pressure −104, r = 0.80). 7. These findings indicate that during continuous endotoxin administration in sheep (1) the renal haemodynamic and functional responses are biphasic, (2) severe impairment of renal function is associated with elevated plasma renin activity and 6-keto-prostaglandin F1α plasma concentrations and with early fatality, and (3) renal filtration capacity directly depends on renal perfusion pressure, suggesting a loss of renal filtration autoregulation during endotoxaemia.

Effect of Sympathetic Nerve Inhibition on the State of Sodium—Volume Balance in Hypertensive Patients with Normal or Impaired Renal Function

1982 ◽  
Vol 63 (s8) ◽  
pp. 301s-303s ◽  
Author(s):  
V. M. Campes ◽  
D. Levitan ◽  
M. S. Romoff ◽  
Y. Saglikes ◽  
I. Sajo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Essential Hypertension ◽  
Impaired Renal Function ◽  
Plasma Renin ◽  
Plasma Noradrenaline ◽  
Mean Blood Pressure ◽  
Volume Balance ◽  
Group 2 ◽  
Group 1

1. The effect of clonidine on the relationship between sympathetic nervous system activity and the state of sodium-volume balance was studied in 15 patients with essential hypertension and normal renal function (group 1) and in 14 patients with hypertension and mild to moderate renal failure (group 2). 2. Acutely, clonidine (200 μg) produced significant falls (P < 0.01) in mean blood pressure, plasma noradrenaline, plasma renin activity and plasma aldosterone in both groups of patients. The changes in mean blood pressure were significantly correlated (P < 0.01) with the changes in plasma noradrenaline. 3. Chronic therapy with clonidine also produced significant falls in mean blood pressure and plasma noradrenaline, but not in plasma renin activity or aldosterone. 4. Exchangeable sodium and plasma volume decreased significantly in patients of group 1 but not in patients of group 2. 5. The data indicate that sympathetic nerve activity may be important for the abnormal relationship between pressure and natriuresis in subjects with essential hypertension and normal renal function, but not in hypertensive subjects with impaired renal function.

Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

1981 ◽  
Vol 60 (4) ◽  
pp. 377-385 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
P. Lijnen
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Sodium Restriction ◽  
Plasma Angiotensin ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar1,Ala8]angiotensin II (saralasin) in man, saralasin was infused in subjects on a ‘normal’ sodium intake (group 1) and during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2), and in sodium-restricted subjects in whom plasma angiotensin II was suppressed by converting-enzyme inhibition with captopril (group 3). 2. The saralasin-induced increase of plasma aldosterone concentration in group 1 was different (P<0.005) from the decrease in group 2, whereas saralasin produced a significant increase of plasma aldosterone in group 3. For the three groups combined the changes of plasma aldosterone were significantly related to control angiotensin II levels, but not to the 24 h urinary sodium excretion. The data suggest that it is the rise of angiotensin II in response to the sodium restriction and not the sodium restriction per se that is associated with the antagonistic action of saralasin on the adrenal receptors. 3. On average mean intra-arterial pressure at 30 min was not affected by saralasin in group 1, had decreased in group 2 and increased (P<0.001) by 4.4 mmHg in group 3. Overall the changes of arterial pressure were significantly related to control angiotensin II, but not to the 24 h sodium excretion, suggesting that the angiotensin II levels predominantly determine the agonistic-antagonistic balance of saralasin's actions on arterial pressure. 4. Although saralasin did not affect plasma renin activity in group 1, plasma renin rose in group 2 and was reduced by 40% (P<0.001) in group 3. For the three groups together the changes of plasma renin activity were significantly related to the changes of mean arterial pressure both on single and multiple regression analyses. The changes of pressure ‘explain’, however, only a fraction of the changes of plasma renin; it is suggested that saralasin has an agonistic effect on the renal receptors involved in the direct suppression of renin by angiotensin II in low-sodium, low-angiotensin conditions and that an antagonistic effect may contribute to the saralasin-induced rise of renin during sodium restriction with appropriate angiotensin II levels.

Abstract 358: Signature microRNA Expression Pattern of Essential Hypertension in a Portuguese Population

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Maria J Pinho ◽  
Manuel Vaz-da-Silva ◽  
Patricio Soares-da- Silva
Keyword(s):  
Essential Hypertension ◽  
Cardiac Disease ◽  
Mononuclear Cells ◽  
Bioinformatic Analysis ◽  
Portuguese Population ◽  
Peripheral Blood Mononuclear ◽  
Group 3 ◽  
Group 2 ◽  
Hybridization Protocol ◽  
Group 1

Hypertension is a complex, multifactorial disease, and its development is determined by a combination of genetic susceptibility and environmental factors. microRNAs have been implicated in numerous biologic processes. Moreover, several studies have demonstrated associations between diseases and specific microRNAs, especially in the cardiovascular system. The present study we assessed the microRNA system in a Portuguese population of hypertensive subjects and explored the potential of microRNAs as biomarkers for essential hypertension. Using Agilent Human miRNA Microarrays, Release 16.0 in combination with a one-color based hybridization protocol and bioinformatic analysis, we determined the microRNA signature of peripheral blood mononuclear cells (PBMCs) from a total of 66 hypertensive subjects (divided into three classes: group 1, medicated HTA I and II; group 2, medicated HTA III; group 3, non-hypertensive with cardiac disease) and 13 non-hypertensive subjects. Bioinformatic analysis revealed 4 miRNAs (miR-4306, miR-146a, miR-22 and miR-146b-5pn) as upregulated not yet related to essential hypertension, and one (miR-186) previously described in myocardial infarction. Endothelial-specific miR-126, nephrosclerosis marker miR-192 and miR-98 (previously implicated in NO and ANP signaling) were found to be upregulated exclusively in group 1 comparing to control. Determining functions and identifying the specific targets of miR-4306, miR-146a, miR-22 and miR-146b-5pn, could determine their value as therapeutic targets for essential hypertension. Supported by FCT (PIC/IC/83204/2007)

scholarly journals INFLUENCE OF HORMONAL DISORDERS ON ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH ARTERIAL HYPERTENSION AND COMORBIDE ENDOCRINOPATHIES

2019 ◽  
Vol 6 (3) ◽  
pp. 132-136
Author(s):  
O. Bilovol ◽  
V. Nemtsova ◽  
I. Ilchenko ◽  
V. Zlatkina
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Subclinical Hypothyroidism ◽  
Control Group ◽  
Group 2 ◽  
Group 1

Abstract. INFLUENCE OF HORMONAL DISORDERS ON ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH ARTERIAL HYPERTENSION AND COMORBIDE ENDOCRINOPATHIES Bilovol O.M., Nemtsova V.D., Ilchenko I.A., Zlatkina V.V. Purpose: to investigate the effect of hormonal changes on endothelial dysfunction (ED) in patients with a comorbid course of hypertension (H), type 2 diabetes mellitus (T2DM) and subclinical hypothyroidism (SHT). Methods: 183 patients with  H stage II were divided into 3 groups: Group 1 (n=50) - with isolated H (comparison group); Group 2 (n=63) - with a combined course of H and T2DM; Group 3 (n=70) - with comorbidity of H, T2DM and SHT. Blood pressure levels, carbohydrate, lipid and thyroid metabolism, plasma insulin concentration, insulin resistance (IR) the HOMA-IR index, vascular endothelial growth factor (VEGF-A) plasma levels were investigated. Results: Dyslipidemia was more pronounced in group 2 than in group 1. The addition of SHT was accompanied by a tendency to increase all the atherogenic lipids. IR was observed in all patients groups and was significantly higher than in control group (p<0.05). Significant increase of VEGF-A levels in all patients groups in comparison with the control (p<0.05) was found. In group 2 VEGF-A was lower than in group 1, which is probably due to the protective effect of metformin. Analysis  of the influence of thyroid dysfunction degree on ED revealed significant increase of VEGF-A levels in TSH>6.0 μMU/ml subgroup (352.55±17.64 pg/ml vs 461.74±20.13 pg/ml (p<0.05)). Conclusion: Hormonal disorders contribute to aggravation of endothelial dysfunction in patients with hypertension and comorbid endocrinopathies - type 2 diabetes mellitus and subclinical hypothyroidism. Even minor decrease in thyroid function lead to the progression of endothelial dysfunction. Key words: hypertension, type 2 diabetes mellitus, subclinical hypothyroidism, endothelial dysfunction   Резюме. ВПЛИВ ГОРМОНАЛЬНИХ ПОРУШЕНЬ НА ЕНДОТЕЛІАЛЬНУ ДИСФУНКЦІЮ УПАЦІЄНТІВ З АРТЕРІАЛЬНОЮ ГІПЕРТЕНЗІЄЮ ТА КОМОРБІДНИМИ ЕНДОКРИНОПАТІЯМИ Біловол О.М., Немцова В.Д., Ільченко І.А., Златкіна В.В. Мета: дослідити вплив гормональних змін на ендотеліальну дисфункцію (ЕД) у пацієнтів з коморбідним перебігом артеріальної гіпертензії (АГ), цукрового діабету 2 типу (ЦД2Т) тасубклінічного гіпотиреозу (СГТ). Матеріали та методи: 183 пацієнта з АГ II стадії були розділені на 3 групи: 1-а група (n=50) - з ізольованою АГ (група порівняння); Група 2 (n=63) - з поєднаним перебігом АГ та ЦД2Т; Група 3 (n 70) – з комбінованим перебігом АГ, ЦД2Т і СГТ. Вивчали рівні артеріального тиску, показники вуглеводного, ліпідного і тиреоїдного обміну, концентрацію інсуліну в плазмі, індекс інсулінорезистентності (ІР) - HOMA-IR, рівні васкулоендотеліального фактора росту (VEGF-A) в плазмі. Результати. Ступінь дисліпідемії у 2-й групі була більш вираженою, ніж в 1-й. Приєднання СГТ супроводжувалося тенденцією до збільшення всіх атерогенних фракцій ліпідів. ІР спостерігалася у всіх групах пацієнтів і була достовірно більше, ніж у контрольній групі (р<0,05). Виявлено достовірне підвищення рівнів VEGF-A у всіх групах пацієнтів в порівнянні з контролем (р<0,05). В 2-й групі рівні VEGF-A були нижче, ніж в 1-й групі, що, ймовірно, пов'язано з протективним ефектом метформіну. Аналіз впливу ступеня гіпофункції щитовидної залози на ЕД виявив значне збільшення рівнів VEGF-A в підгрупі TSH> 6,0 мкМ / мл (352,55 ± 17,64 пг / мл і 461,74 ± 20,13 пг / мл відповідно, р <0,05). Висновки. Гормональні порушення сприяють погіршенню ендотеліальної дисфункції у пацієнтів з артеріальною гіпертензією та супутніми ендокринопатіями - цукровим діабетом 2 типу та субклінічним гіпотиреозом. Навіть незначне зниження функції щитовидної залози призводить до прогресування ендотеліальної дисфункції. Ключові слова:  гіпертензія, цукровий діабет 2 тип, субклінічний гіпотиреоз, ендотеліальна дисфункція    Резюме. ВЛИЯНИЕ ГОРМОНАЛЬНЫХ НАРУШЕНИЙ НА ЭНДОТЕЛИАЛЬНУЮ ДИСФУНКЦИЮ У ПАЦИЕНТОВ С АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИЕЙ И КОМОРБИДНЫМИ ЭНДОКРИНОПАТИЯМИ Беловол О.М., Немцова В.Д., Ильченко И.А., Златкина В.В. Цель: исследовать влияние гормональных изменений на эндотелиальную дисфункцию (ЭД) у пациентов с коморбидным течением артериальной гипертензии (АГ), сахарного диабета 2 типа (СД2Т) и субклинического гипотиреоза (СГТ). Материалы и методы: 183 пациента с АГ IIстадии были разделены на 3 группы: 1-я группа (n = 50) - с изолированной АГ (группа сравнения); Группа 2 (n = 63) - с сочетанным течением АГ и СД2Т; Группа 3 (n = 70) - комбинированное течение АГ, СД2Т и СГТ. Изучали уровни артериального давления,  показатели  углеводного, липидного и тиреоидного обмена, концентрацию инсулина в плазме, индекс инсулинорезистентности (ИР)- HOMA-IR, уровни васкулоэндотелиального фактора роста(VEGF-A) в плазме. Результаты. Степень дислипидемии во 2-й группе была более выраженной, чем в 1-й.  Присоединение СГТ сопровождалось тенденцией к увеличению всех атерогенных фракций липидов. ИР наблюдалась во всех группах пациентов и была достоверно больше, чем в контрольной группе (р<0,05). Выявлено достоверное повышение уровней VEGF-A во всех группах пациентов по сравнению с контролем (р <0,05). Во 2-й группе уровни VEGF-A были ниже, чем в 1-й группе, что, вероятно, связано с протективным эффектом метформина. Анализ влияния степени дисфункции щитовидной железы на ЭД выявил значительное увеличение уровней VEGF-A в подгруппе TSH> 6,0 мкМ/мл (352,55 ± 17,64 пг / мл и 461,74 ± 20,13 пг / мл соответственно, р<0,05). Заключение. Гормональные нарушения способствуют ухудшению эндотелиальной дисфункции у пациентов с артериальной гипертензией и сопутствующими эндокринопатиями - сахарным диабетом 2 типа и субклиническим гипотиреозом. Даже незначительное снижение функции щитовидной железы приводит к прогрессированию эндотелиальной дисфункции. Ключевые слова: гипертензия, сахарный диабет 2 тип, субклинический гипотиреоз, эндотелиальная дисфункция     

scholarly journals The effect of hormonal disbalance on the aging rate change in the patients with arterial hypertension and comorbid endocrinopathies

2019 ◽  
Vol 23 (2) ◽  
pp. 277-282
Author(s):  
V. D. Nemtsova ◽  
I. A. Ilchenko ◽  
V. V. Zlatkina
Keyword(s):  
Arterial Hypertension ◽  
Premature Aging ◽  
Endocrine Disorders ◽  
Anthropometric Parameters ◽  
Aging Rate ◽  
Age Related ◽  
Number Of Patients ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Due to the growing number of patients with age-related diseases, the aim of the study was to investigate in the changes of aging rate (AR) in patients with comorbid course of arterial hypertension (H), type 2 diabetes mellitus (T2DM) and subclinical hypothyroidism (SH) and to study the features of these changes depending on hormonal imbalance. 118 patients (63 women and 55 men, average age — 53.6±4.3 years) were divided into 3 groups: group 1 (n=37) with isolated H; group 2 (n=42) — with H and T2DM; group 3 (n=39) — with H, T2DM and SH. The investigation program included: measurement of anthropometric parameters (blood pressure, height, body weight (BW), body mass index (BMI)), carbohydrate and thyroid metabolism using standard methods, biological age (BA) by V.P. Voitenko et al. Statistical processing was performed using the Statistica for Windows 8.0 software package. When evaluating AR, physiological aging was found in 8 patients (21.6%) of group 1, in 4 (9.5%) patients of group 2 and 3 (7.7%) of patients in group 3. In the overwhelming majority of the examined patients, premature aging (PA) was noted, however, the acceleration of PA between patients of groups 2 and 3 was not differ significantly (p>0.05). The increase in AR in group 2 patients was accompanied by an increase in BA by 7.2 years, in 3 group patients — by 7.3 years compared with their chronological age. A correlation analysis revealed a positive relationship between BMI and coefficient of aging rate (CAR) (r=0.679; p<0.05); BMI and BA (r=0.562; p<0.05) and CAR and the TSH level (r=0.050; p=0.388) in the 3rd group. Thus, the presence of hypertension and comorbid endocrinopathies — T2DM and SH significantly increases the AR and when assessing the effect of endocrine disorders, the presence of T2DM is more important than SH.

scholarly journals Glycopenia - induced sympathoadrenal activation in diabetes mellitus and uncontrolled arterial hypertension: an observational study

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Abimbola Abobarin-Adeagbo ◽  
Andreas Wienke ◽  
Matthias Girndt ◽  
Rainer U. Pliquett
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Insulin Dose ◽  
Hypertensive Crisis ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Group 3 ◽  
Group 2 ◽  
Group 1 ◽  
Diabetes Patients

Abstract Background Aim of this study is to investigate a possible association of hypoglycemic episodes and arterial hypertension. We hypothesize that hospitalized insulin-treated diabetes patients with hypertensive crisis have more hypoglycemic episodes than their counterparts without hypertensive crisis on admission. Methods In a prospective, observational cohort study, 65 insulin-treated diabetes patients (type 1, type 2, type 3c) were included in Group 1, when a hypertensive crisis was present, as control patients in Group 2 without hypertensive crisis or hypoglycemia, in Group 3, when a symptomatic hypoglycemia was present on admission. All patients were subjected to open-label continuous glucose monitoring, 24-h blood-pressure- and Holter electrocardiogram recordings, and to laboratory tests including plasma catecholamines. Results 53 patients, thereof 19 Group-1, 19 Group-2, 15 Group-3 patients, completed this study. Group-1 patients had the highest maximum systolic blood pressure, a higher daily cumulative insulin dose at admission, a higher body-mass index, and a higher plasma norepinephrine than control patients of Group 2. Group-3 patients had more documented hypoglycemic episodes (0.8 ± 0.5 per 24 h) than Group-2 patients (0.2 ± 0.3 per 24 h), however, they were not different to the ones in Group-1 patients (0.4 ± 0.4 per 24 h). Plasma norepinephrine and mean arterial blood pressure were higher Group-1 and Group-3 patients than in control patients of Group 2. At discharge, the daily cumulative insulin dose was reduced in Group-1 (− 18.4 ± 24.9 units) and in Group-3 patients (− 18.6 ± 22.7 units), but remained unchanged in Group-2 control patients (− 2.9 ± 15.6 units). Conclusions An association between hypoglycemic events and uncontrolled hypertension was found in this study.

Cardiovascular and renal actions of C-type natriuretic peptide

1992 ◽  
Vol 262 (1) ◽  
pp. H308-H312 ◽  
Author(s):  
A. J. Stingo ◽  
A. L. Clavell ◽  
L. L. Aarhus ◽  
J. C. Burnett
Keyword(s):  
Arterial Pressure ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Sodium Reabsorption ◽  
Bolus Administration ◽  
Systemic Hemodynamic ◽  
Biological Responses ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Group 1

Studies were performed in two groups of anesthetized dogs (n = 5 per group) to determine the cardiovascular and renal actions of synthetic C-type natriuretic peptide (CNP). Systemic infusion of CNP (group 1; 10 and 50 ng.kg-1.min-1 iv) resulted in marked cardiovascular hemodynamic effects characterized by a decrease in mean arterial pressure, cardiac output, and atrial pressures in association with a decrease in sodium excretion. Bolus administration of CNP (group 2; 5 micrograms/kg iv) to minimize cardiovascular hemodynamic changes resulted in only a transient decrease in arterial pressure. Sodium excretion decreased despite a return of arterial pressure to baseline. These biological responses were associated with increases in plasma guanosine 3',5'-cyclic monophosphate (cGMP) in both groups but with no change in urinary cGMP. With both systemic infusion or bolus administration of CNP, significant increases in plasma aldosterone were observed in association with increases in distal nephron sodium reabsorption. This study demonstrates that CNP exhibits profound systemic hemodynamic actions and is indirectly, or perhaps directly, antinatriuretic.

scholarly journals Reducing TRPC1 Expression through Liposome-Mediated siRNA Delivery Markedly Attenuates Hypoxia-Induced Pulmonary Arterial Hypertension in a Murine Model

2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Cheuk-Kwan Sun ◽  
Yen-Yi Zhen ◽  
Hung-I Lu ◽  
Pei-Hsun Sung ◽  
Li-Teh Chang ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Similar Pattern ◽  
Sirna Delivery ◽  
Opposite Pattern ◽  
Protein Expressions ◽  
Pulmonary Arterial ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

We tested the hypothesis that Lipofectamine siRNA delivery to deplete transient receptor potential cation channel (TRPC) 1 protein expression can suppress hypoxia-induced pulmonary arterial hypertension (PAH) in mice. Adult male C57BL/6 mice were equally divided into group 1 (normal controls), group 2 (hypoxia), and group 3 (hypoxia + siRNA TRPC1). By day 28, right ventricular systolic pressure (RVSP), number of muscularized arteries, right ventricle (RV), and lung weights were increased in group 2 than in group 1 and reduced in group 3 compared with group 2. Pulmonary crowded score showed similar pattern, whereas number of alveolar sacs exhibited an opposite pattern compared to that of RVSP in all groups. Protein expressions of TRPCs, HIF-1α, Ku-70, apoptosis, and fibrosis and pulmonary mRNA expressions of inflammatory markers were similar pattern, whereas protein expressions of antifibrosis and VEGF were opposite to the pattern of RVSP. Cellular markers of pulmonary DNA damage, repair, and smooth muscle proliferation exhibited a pattern similar to that of RVSP. The mRNA expressions of proapoptotic and hypertrophy biomarkers displayed a similar pattern, whereas sarcomere length showed an opposite pattern compared to that of RVSP in all groups. Lipofectamine siRNA delivery effectively reduced TRPC1 expression, thereby attenuating PAH-associated RV and pulmonary arteriolar remodeling.

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