scholarly journals Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Iveta Bernatova
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Mechanisms Of Action ◽  
Experimental Models ◽  
Experimental Hypertension ◽  
Vascular Bed ◽  
Induced Hypertension

Hypertension is a risk factor for other cardiovascular diseases and endothelial dysfunction was found in humans as well as in various commonly employed animal experimental models of arterial hypertension. Data from the literature indicate that, in general, endothelial dysfunction would not be the cause of experimental hypertension and may rather be secondary, that is, resulting from high blood pressure (BP). The initial mechanism of endothelial dysfunction itself may be associated with a lack of endothelium-derived relaxing factors (mainly nitric oxide) and/or accentuation of various endothelium-derived constricting factors. The involvement and role of endothelium-derived factors in the development of endothelial dysfunction in individual experimental models of hypertension may vary, depending on the triggering stimulus, strain, age, and vascular bed investigated. This brief review was focused on the participation of endothelial dysfunction, individual endothelium-derived factors, and their mechanisms of action in the development of high BP in the most frequently used rodent experimental models of arterial hypertension, including nitric oxide deficient models, spontaneous (pre)hypertension, stress-induced hypertension, and selected pharmacological and diet-induced models.

scholarly journals Vascular and renal function in experimental thyroid disorders

2006 ◽  
Vol 154 (2) ◽  
pp. 197-212 ◽  
Author(s):  
Félix Vargas ◽  
Juan Manuel Moreno ◽  
Isabel Rodríguez-Gómez ◽  
Rosemary Wangensteen ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Thyroid Hormones ◽  
Arterial Hypertension ◽  
Vascular Resistance ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Experimental Hypertension ◽  
Water Metabolism

This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper- and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the reninangiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

Evaluation of the Effects of a Pinus Brutia Bark Extract on Biochemical Parameters and Blood Pressure in an Experimental Arterial Hypertension

2018 ◽  
Vol 69 (7) ◽  
pp. 1718-1721 ◽  
Author(s):  
Catrinel Florentina Paduraru(Giurescu Bedreag) ◽  
Nina Filip ◽  
Adriana Trifan ◽  
Sorin Dan Miron ◽  
Codruta Badescu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Biochemical Parameters ◽  
Bark Extract ◽  
Pinus Brutia ◽  
Target Organs ◽  
Induced Hypertension ◽  
Oxidative Effects ◽  
And Oxidative Stress

The new hypertension therapies which are thought to improve the mechanisms impairing the target organs in arterial hypertension (AHT) would have great practical value. The aim of our study was to investigate the effects of Pinus brutia bark extract (EPb) on serum lipid profiles and oxidative stress in N(G)-Nitro-L-arginine-methyl ester (L-NAME)-induced hypertension. The experiment demonstrated that PbE improved lipid profile and reduced pro-oxidative effects of L-NAME, thus suggesting a possible role of the extract in the management of AHT. Systolic and diastolic blood pressure decrease was significant in the group undergoing simultaneous EPb extract and L-NAME therapy, as compared to the group that was administered only L-NAME. Due to its effects, the Pinus brutia bark extract may be used for the prophylaxis and as adjuvant therapy of cardiovascular conditions.

Hemodynamic effects ofl-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors

1998 ◽  
Vol 274 (4) ◽  
pp. H1066-H1074 ◽  
Author(s):  
Eduardo Colombari ◽  
Robin L. Davisson ◽  
Richard A. Shaffer ◽  
William T. Talman ◽  
Stephen J. Lewis
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Pressor Response ◽  
Nitric Oxide Synthesis ◽  
Hemodynamic Effects ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Sympathetic Nervous

This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of l-glutamate (l-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection ofl-Glu produced an initial pressor response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, l-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of l-Glu after administration of prazosin and N G-nitro-l-arginine methyl ester (l-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections ofl-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of l-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Effect of magnesium supplementation on blood pressure and vascular reactivity in nitric oxide synthase inhibition-induced hypertension model

2015 ◽  
Vol 37 (8) ◽  
pp. 633-642 ◽  
Author(s):  
Filiz Basralı ◽  
Günnur Koçer ◽  
Pınar Ülker Karadamar ◽  
Seher Nasırcılar Ülker ◽  
Leyla Satı ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Magnesium Supplementation ◽  
Induced Hypertension ◽  
Oxide Synthase

scholarly journals Nitric oxide synthase-mediated blood pressure regulation in obese melanocortin-4 receptor-deficient pregnant rats

2016 ◽  
Vol 311 (5) ◽  
pp. R851-R857 ◽  
Author(s):  
Frank T. Spradley ◽  
Jennifer M. Sasser ◽  
Jacqueline B. Musall ◽  
Jennifer C. Sullivan ◽  
Joey P. Granger
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mesenteric Arteries ◽  
Elevated Blood Pressure ◽  
Pressure Regulation ◽  
Elevated Blood ◽  
Pregnant Rats ◽  
Melanocortin 4 Receptor ◽  
Regulation Of Blood Pressure

Although obesity increases the risk for hypertension in pregnancy, the mechanisms responsible are unknown. Increased nitric oxide (NO) production results in vasodilation and reduced blood pressure during normal pregnancy in lean rats; however, the role of NO is less clear during obese pregnancies. We examined the impact of obesity on NO synthase (NOS)-mediated regulation of blood pressure during pregnancy by testing the hypothesis that NOS activity, expression, and regulation of vascular tone and blood pressure are reduced in obese pregnant rats. At gestational day 19, melanocortin-4 receptor (MC4R)-deficient obese rats (MC4R) had greater body weight and fat mass with elevated blood pressure and circulating sFlt-1 levels compared with MC4R pregnant rats. MC4R pregnant rats also had less circulating cGMP levels and reduced total NOS enzymatic activity and expression in mesenteric arteries. Despite decreased biochemical measures of NO/NOS in MC4R rats, NOS inhibition enhanced vasoconstriction only in mesenteric arteries from MC4R rats, suggesting greater NOS-mediated tone. To examine the role of NOS on blood pressure regulation in obese pregnant rats, MC4R and MC4R pregnant rats were administered the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 100 mg/l) from gestational day 14 to 19 in drinking water. The degree by which l-NAME raised blood pressure was similar between obese and lean pregnant rats. Although MC4R obese pregnant rats had elevated blood pressure associated with reduced total NOS activity and expression, they had enhanced NOS-mediated attenuation of vasoconstriction, with no evidence of alterations in NOS-mediated regulation of blood pressure.

Cardiac baroreflex dysfunction in patients with pulmonary arterial hypertension at rest and during orthostatic stress: Role of the peripheral chemoreflex

2021 ◽  
Author(s):  
Marcelle Paula-Ribeiro ◽  
Indyanara C. Ribeiro ◽  
Liliane C. Aranda ◽  
Talita M. Silva ◽  
Camila M. Costa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Early Stage ◽  
Pressure Fluctuations ◽  
Sit To Stand ◽  
Peak Aerobic Capacity ◽  
Pulmonary Arterial ◽  
Peripheral Chemoreflex

The baroreflex integrity in early-stage pulmonary arterial hypertension (PAH) remains uninvestigated. A potential baroreflex impairment could be functionally relevant and possibly mediated by enhanced peripheral chemoreflex activity. Thus, we investigated 1) the cardiac baroreflex in non-hypoxemic PAH; 2) the association between baroreflex indexes and peak aerobic capacity (i.e., V̇O2peak); and 3) the peripheral chemoreflex contribution to the cardiac baroreflex. Nineteen patients and 13 age- and sex-matched healthy adults (HA) randomly inhaled either 100% O2 (peripheral chemoreceptors inhibition) or 21% O2 (control session), while at rest and during a repeated sit-to-stand maneuver. Beat-by-beat analysis of R-R intervals and systolic blood pressure provided indexes of cardiac baroreflex sensitivity (cBRS) and effectiveness (cBEI). The PAH group had lower cBEIALL at rest (mean ± SD: PAH = 0.5 ± 0.2 vs HA = 0.7 ± 0.1 a.u., P = 0.02) and lower cBRSALL (PAH = 6.8 ± 7.0 vs HA = 9.7 ± 5.0 ms mmHg-1, P < 0.01) and cBEIALL (PAH = 0.4 ± 0.2 vs HA= 0.6 ± 0.1 a.u., P < 0.01) during the sit-to-stand maneuver versus the HA group. The cBEI during the sit-to-stand maneuver was independently correlated to V̇O2peak (partial r = 0.45, P < 0.01). Hyperoxia increased cBRS and cBEI similarly in both groups at rest and during the sit-to-stand maneuver. Therefore, cardiac baroreflex dysfunction was observed under spontaneous and, most notably, provoked blood pressure fluctuations in non-hypoxemic PAH, was not influenced by the peripheral chemoreflex, and was associated with lower V̇O2peak suggesting it could be functionally relevant.

scholarly journals The Role of Uridine Adenosine Tetraphosphate in the Vascular System

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Rita C. Tostes ◽  
R. Clinton Webb
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Smooth Muscle Cells ◽  
Vascular Function ◽  
Purinergic Receptors ◽  
Potential Role ◽  
Vascular System

The endothelium plays a pivotal role in vascular homeostasis, and endothelial dysfunction is a major feature of cardiovascular diseases, such as arterial hypertension, atherosclerosis, and diabetes. Recently, uridine adenosine tetraphosphate (Up4A) has been identified as a novel and potent endothelium-derived contracting factor (EDCF). Up4A structurally contains both purine and pyrimidine moieties, which activate purinergic receptors. There is an accumulating body of evidence to show that Up4A modulates vascular function by actions on endothelial and smooth muscle cells. In this paper, we discuss the effects of Up4A on vascular function and a potential role for Up4A in cardiovascular diseases.

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