Vasoactive Factors and Blood Pressure in Children

2013 ◽  
pp. 25-41
Author(s):  
Ihor V. Yosypiv
Author(s):  
Husam Ghanim ◽  
Manav Batra ◽  
Kelly Green ◽  
Jeanne Hejna ◽  
Sanaa Abuaysheh ◽  
...  

2006 ◽  
Vol 291 (2) ◽  
pp. E268-E274 ◽  
Author(s):  
Arvi Duka ◽  
Irena Duka ◽  
Guohong Gao ◽  
Sherene Shenouda ◽  
Irene Gavras ◽  
...  

With inhibition or absence of the bradykinin B2 receptor (B2R), B1R is upregulated and assumes some of the hemodynamic properties of B2R, indicating that both participate in the maintenance of normal vasoregulation or to development of hypertension. Herein we further evaluate the role of bradykinin in normal blood pressure (BP) regulation and its relationship with other vasoactive factors by selectively blocking its receptors. Six groups of Wistar rats were treated for 3 wk: one control group with vehicle alone, one with concurrent administration of B1R antagonist R-954 (70 μg·kg−1·day−1) and B2R antagonist HOE-140 (500 μg·kg−1·day−1), one with R-954 alone, one with HOE 140 alone, one with concurrent administration of both R-954 and HOE-140 plus the angiotensin antagonist losartan (5 mg·kg−1·day−1), and one with only losartan. BP was measured continuously by radiotelemetry. Only combined administration of B1R and B2R antagonists produced a significant BP increase from a baseline of 107–119 mmHg at end point, which could be partly prevented by losartan and was not associated with change in catecholamines, suggesting no involvement of the sympathoadrenal system. The impact of blockade of bradykinin on other vasoregulating systems was assessed by evaluating gene expression of different vasoactive factors. There was upregulation of the eNOS, AT1 receptor, PGE2 receptor, and tissue kallikrein genes in cardiac and renal tissues, more pronounced when both bradykinin receptors were blocked; significant downregulation of AT2 receptor gene in renal tissues only; and no consistent changes in B1R and B2R genes in either tissue. The results indicate that both B1R and B2R contribute to the maintenance of normal BP, but one can compensate for inhibition of the other, and the chronic inhibition of both leads to significant upregulation in the genes of related vasoactive systems.


2014 ◽  
Vol 307 (12) ◽  
pp. E1085-E1096 ◽  
Author(s):  
Patricia Martínez-Miguel ◽  
Jose Manuel Valdivielso ◽  
Diana Medrano-Andrés ◽  
Pablo Román-García ◽  
Jose Luis Cano-Peñalver ◽  
...  

Despite the presence of vitamin D receptor (VDR) in endothelial cells, the effect of vitamin D on endothelial function is unknown. An unbalanced production of vasoactive endothelial factors such as nitric oxide (NO) or endothelin-1 (ET-1) results in endothelial dysfunction, which can alter the normal cardiovascular function. Present experiments were devoted to assess the effect of active vitamin D (calcitriol) on the synthesis of endothelial vasoactive factors. The results were that, in cells, calcitriol increased ET-1 and NO productions, which were measured by ELISA and fluorimetric assay, respectively. Calcitriol also increased endothelin-converting enzyme-1 (ECE-1) and endothelial-nitric oxide synthase (eNOS) activities, their mRNA (qPCR), their protein expressions (Western-blot), and their promoter activities (transfection assays). Calcitriol did not change prepro-ET-1 mRNA. The effect was specific to VDR activation because when VDR was silenced by siRNA, the observed effects disappeared. Mechanisms involved in each upregulation differed. ECE-1 upregulation depended on AP-1 activation, whereas eNOS upregulation depended directly on VDR activation. To evaluate the in vivo consequences of acute calcitriol treatment, normal Wistar rats were treated with a single ip injection of 400 ng/kg calcitriol and euthanized 24 h later. Results confirmed those observed in cells, that production and expression of both factors were increased by calcitriol. Besides, calcitriol-treated rats showed a slight rise in mean blood pressure, which decreased when pretreated with FR-901533, an ECE-1 antagonist. We conclude that calcitriol increases the synthesis of both ET-1 and NO in endothelial cells. However, the ET-1 upregulation seems to be biologically more relevant, as animals acutely treated with calcitriol show slight increases in blood pressure.


2013 ◽  
Vol 82 (1) ◽  
pp. 103-107 ◽  
Author(s):  
De-Zhang Lu ◽  
Hong-Gang Fan ◽  
Sheng Jiang ◽  
Li-Juan Tan ◽  
Shi-Ming Yu ◽  
...  

This study focused on anaesthesia and cardiopulmonary effects of tiletamine-zolazepam/xylazine/tramadol in miniature pigs and its effects on endothelium-derived vasoactive factors. A total of 14 eight-month-old Chinese experimental miniature pigs were used in this study. Tiletamine-zolazepam (3.5 mg·kg-1), xylazine (1.32 mg·kg-1) and tramadol (1.8 mg·kg-1) were administered i.m.; blood pressure and heart rate were recorded. At the same time, blood was collected through precaval vein, and nitric oxide, endothelin, 6-keto-PGF1α and thromboxanes B2 were determined by colorimetry and radioimmunoassay. The mean times to dorsal recumbency, duration of immobilization, standing and walking were 2.26 ± 0.72, 87.57 ± 9.61, 25.63 ± 12.55 and 36.70 ± 14.53 min, respectively. Blood pressure was significantly changed at 10 and 80 min (P < 0.01), and the heart rate ranged from 89 to 134 bpm without episodes of severe bradycardia or tachycardia. Significantly positive correlation was observed between endothelin, thromboxanes B2 and blood pressure as well as the heart rate (P < 0.05). There was negative correlation between PGI2 and blood pressure as well as heart rate (P < 0.05). The results showed that endothelin, 6-keto-PGF1α and thromboxanes B2 participated in the changing of cardiopulmonary parameters which were caused by tiletamine-zolazepam-xylazine-tramadol anaesthesia in miniature pigs, and the 6-keto-PGF1α, ET and TXB2 concentrations in plasma participated in the changing of blood pressures during anaesthesia. Therefore, we can recommend tiletamine-zolazepam/xylazine/tramadol for anaesthesia in pigs, and this study also contributes to the evaluation of the effect of endothelium-derived vasoactive factors during anaesthesia.


Physiology ◽  
1989 ◽  
Vol 4 (2) ◽  
pp. 64-68
Author(s):  
JAF Tresguerres ◽  
V Lahera ◽  
MV Cachofeiro

A high intake of polyunsaturated fatty acids has been reported as being able to reduce blood pressure and to protect against several cardiovascular diseases. These effects have been observed in hypertensive and normotensive humans and in experimental models of hypertension. Prostaglandins have been considered responsible for these beneficial effects, although other vasoactive factors could also be involved.


2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Jochen Stenzel ◽  
Sebastian Noe ◽  
Konstantin Holzapfel ◽  
Franziska Erlmeier ◽  
Florian Eyer

An increased release of serotonin secreted by ileal NETs is thought to be the major factor causing the carcinoid syndrome. However, in acutely arising carcinoid crisis also other vasoactive factors may lead to hazardous fluctuations in blood pressure and bronchial constriction. In rare cases, systemic vasoconstriction can be observed, probably caused by catecholamines or similar acting substances. Here, we report a fatal case of fulminant systemic vasoconstriction possibly caused by catecholamines in a patient with metastasized ileal NET. The vasospasm was detected by CT-angiography, and hemodynamic monitoring revealed a high systemic vascular resistance. Epinephrine, norepinephrine, and chromogranin A levels in plasma were elevated as was the urinary 5-hydroxyindoleacetic acid (5-HIAA). The cause of death was heart failure due to severe circulatory insufficiency. The progression of the tumor disease was confirmed by autopsy.


1988 ◽  
Vol 52 (9) ◽  
pp. 519-521
Author(s):  
NK Nordstrom ◽  
S Longenecker ◽  
HL Whitacre ◽  
FM Beck

Sign in / Sign up

Export Citation Format

Share Document