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Article ; Online: Haemodynamic effects of the flavonoid quercetin in rats revisited.

Vrolijk, Misha F / van Essen, Helma / Opperhuizen, Antoon / Bast, Aalt / Janssen, Ben J

2020 Volume 177, Issue 8, Page(s) 1841–1852

Abstract: Background and purpose: The flavonoid quercetin increased the in vitro potency of the α: Experimental approach: First, in rats pretreated with quercetin or its vehicle, responses to phenylephrine and tamsulosin were examined. Second, tamsulosin- ... ...

Abstract	Background and purpose: The flavonoid quercetin increased the in vitro potency of the α Experimental approach: First, in rats pretreated with quercetin or its vehicle, responses to phenylephrine and tamsulosin were examined. Second, tamsulosin-induced changes in renal, mesenteric, hindquarter and carotid conductance were compared in quercetin- and vehicle-treated rats instrumented with Doppler flow probes. Animals were also placed on a tilt table to record regional haemodynamic changes to orthostatic challenges. Third, adult SHR were instrumented with telemeters to measure 24-hr patterns of BP. Recordings were made before and during a 5-week oral treatment of quercetin. Finally, pre-hypertensive SHR were treated with quercetin from 4 to 8 weeks of age and arterial pressure was measured at 8 and 12 weeks. Key results: Pretreatment with quercetin did not influence the responses to phenylephrine and tamsulosin, in neither WKY nor SHR. While tamsulosin treatment and tilting lowered BP and increased conductance in all vascular beds, effect size was not influenced by pretreatment with quercetin. Prolonged treatment with quercetin, in either prehypertensive SHR or adult SHR with established hypertension did not lower BP. Conclusions and implications: Cumulatively, these data demonstrate that quercetin does not amplify haemodynamic effects of tamsulosin or tilting in vivo in rats and has no effect on BP development in SHR.
MeSH term(s)	Animals ; Blood Pressure ; Flavonoids ; Hemodynamics ; Hypertension/drug therapy ; Quercetin/pharmacology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY
Chemical Substances	Flavonoids ; Quercetin (9IKM0I5T1E)
Language	English
Publishing date	2020-02-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.14955
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Article ; Online: Amlodipine limits microglia activation and cognitive dysfunction in aged hypertensive mice.

Kerkhofs, Danielle / Helgers, Robin / Hermes, Denise / Steinbusch, Hellen P J / Van Essen, Helma / Leenders, Peter / Prickaerts, Jos / Staals, Julie / Biessen, Erik A / Van Oostenbrugge, Robert J / Foulquier, Sébastien

Journal of hypertension

2023 Volume 41, Issue 7, Page(s) 1159–1167

Abstract: Background: SBP and blood pressure variability are independent risk factors for cerebral small vessel disease, a leading cause for stroke and dementia. Calcium-channel blockers are known to reduce blood pressure variability and may thus offer benefit ... ...

Abstract	Background: SBP and blood pressure variability are independent risk factors for cerebral small vessel disease, a leading cause for stroke and dementia. Calcium-channel blockers are known to reduce blood pressure variability and may thus offer benefit against dementia. Beyond this effect, the impact of calcium-channel blockers on hypertension-induced neuroinflammation, and especially, microglial phenotype remains unknown. We aimed to study the ability of amlopidine to alleviate microglia inflammation, and slow down cognitive dysfunction in aged hypertensive mice. Methods: Hypertensive BPH/2J and normotensive BPN/3J mice were studied until 12 months of age. Hypertensive mice were untreated or received amlodipine (10 mg/kg per day). Blood pressure parameters were measured by telemetry and tail cuff plethysmography. Mice underwent repeated series of cognitive tasks. Brain immunohistochemistry was performed to study blood-brain barrier dysfunction and microglial pro-inflammatory phenotype (CD68 + Iba1 + cells; morphological analysis). Results: Amlodipine normalized SBP over the entire life span and decreased blood pressure variability. BPH/2J mice exhibited impaired short-term memory that was prevented by amlodipine at 12 months (discrimination index 0.41 ± 0.25 in amlodipine-treated vs. 0.14 ± 0.15 in untreated BPH/2J mice, P = 0.02). Amlopidine treatment of BPH/2J did not prevent blood-brain barrier leakage, a measure of cerebral small vessel disease, but limited its size. Microglia's inflammatory phenotype in BPH/2J, characterized by an increased number of Iba1 + CD68 + cells, increased soma size and shortened processes, was partly reduced by amlodipine. Conclusion: Amlodipine attenuated the short-term memory impairment in aged hypertensive mice. Beyond its blood pressure lowering capacity, amlodipine may be cerebroprotective by modulating neuroinflammation.
MeSH term(s)	Animals ; Mice ; Amlodipine/pharmacology ; Amlodipine/therapeutic use ; Antihypertensive Agents/pharmacology ; Antihypertensive Agents/therapeutic use ; Blood Pressure/physiology ; Calcium ; Calcium Channel Blockers/therapeutic use ; Dementia ; Hypertension/complications ; Hypertension/drug therapy ; Hypertension/genetics ; Microglia ; Neuroinflammatory Diseases
Chemical Substances	Amlodipine (1J444QC288) ; Antihypertensive Agents ; Calcium (SY7Q814VUP) ; Calcium Channel Blockers
Language	English
Publishing date	2023-04-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000003445
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Zs.A 1885: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Pharmacological depletion of microglia and perivascular macrophages prevents Vascular Cognitive Impairment in Ang II-induced hypertension.

Kerkhofs, Danielle / van Hagen, Britt T / Milanova, Irina V / Schell, Kimberly J / van Essen, Helma / Wijnands, Erwin / Goossens, Pieter / Blankesteijn, W Matthijs / Unger, Thomas / Prickaerts, Jos / Biessen, Erik A / van Oostenbrugge, Robert J / Foulquier, Sébastien

Theranostics

2020 Volume 10, Issue 21, Page(s) 9512–9527

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Blood Pressure/drug effects ; Blood-Brain Barrier/metabolism ; Brain/drug effects ; Brain/metabolism ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/prevention & control ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Hypertension/chemically induced ; Hypertension/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice ; Microglia/drug effects ; Microglia/metabolism ; Organic Chemicals/pharmacology
Chemical Substances	Enzyme Inhibitors ; Organic Chemicals ; PLX5622 ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2020-07-25
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.44394
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Article ; Online: Renal inflammatory markers during the onset of hypertension in spontaneously hypertensive rats.

Heijnen, Bart Fj / Van Essen, Helma / Schalkwijk, Casper G / Janssen, Ben Ja / Struijker-Boudier, Harry Aj

Hypertension research : official journal of the Japanese Society of Hypertension

2014 Volume 37, Issue 2, Page(s) 100–109

Abstract: Early blockade of the renin-angiotensin system is successful in delaying the development of hypertension in spontaneously hypertensive rats (SHRs) and ameliorating organ damage by inhibition of the inflammatory response. In this study, we investigated ... ...

Abstract	Early blockade of the renin-angiotensin system is successful in delaying the development of hypertension in spontaneously hypertensive rats (SHRs) and ameliorating organ damage by inhibition of the inflammatory response. In this study, we investigated the role of the angiotensin II type 1 receptor (AT1R) in the early renal inflammatory response in SHR. Blood pressure development and renal inflammatory markers were measured in 4-, 8- and 12-week-old SHR and age-matched Wistar Kyoto (WKY) rats. Separate groups of SHRs were transiently treated with the AT1R blocker losartan between 4 and 8 weeks of age. Urinary excretion of the renal injury markers osteopontin and neutrophil gelatinase-associated lipocalin increased in young SHR. Further, renal expression of inflammatory genes was also increased in young SHR. Losartan inhibited the increase of these inflammatory markers. In contrast, gene expression of the renal injury marker and T-cell inducer kidney injury molecule-1 (KIM-1) was reduced in 4-week-old SHR when compared with WKY. Similarly, the T-cell marker CD3 was significantly decreased in 4-week-old SHR. These effects were not antagonized by AT1R blockade. This study confirms the presence of an early renal inflammatory response in SHR that can be blocked by AT1R antagonism. In addition, it demonstrates that KIM-1 does not behave as a pure kidney injury marker in young SHR, but may reflect kidney maturation.
MeSH term(s)	Adaptive Immunity/physiology ; Angiotensin II Type 1 Receptor Blockers/therapeutic use ; Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Biomarkers/metabolism ; Biomarkers/urine ; CD3 Complex/metabolism ; Gene Expression ; Hemodynamics/physiology ; Hypertension/genetics ; Hypertension/metabolism ; Immunohistochemistry ; Inflammation/metabolism ; Kidney/metabolism ; Kidney Function Tests ; Losartan/therapeutic use ; Male ; Polymerase Chain Reaction ; RNA/biosynthesis ; RNA/genetics ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptor, Angiotensin, Type 1/biosynthesis ; Receptor, Angiotensin, Type 1/genetics ; Renin-Angiotensin System/physiology
Chemical Substances	Angiotensin II Type 1 Receptor Blockers ; Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; Biomarkers ; CD3 Complex ; CD68 antigen, human ; Receptor, Angiotensin, Type 1 ; RNA (63231-63-0) ; Losartan (JMS50MPO89)
Language	English
Publishing date	2014-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1175297-x
ISSN	1348-4214 ; 0916-9636
ISSN (online)	1348-4214
ISSN	0916-9636
DOI	10.1038/hr.2013.99
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Article ; Online: Irreversible renal damage after transient renin-angiotensin system stimulation: involvement of an AT1-receptor mediated immune response.

Heijnen, Bart F J / Nelissen, Jelly / van Essen, Helma / Fazzi, Gregorio E / Cohen Tervaert, Jan W / Peutz-Kootstra, Carine J / Mullins, John J / Schalkwijk, Casper G / Janssen, Ben J A / Struijker-Boudier, Harry A J

PloS one

2013 Volume 8, Issue 2, Page(s) e57815

Abstract: Transient activation of the renin-angiotensin system (RAS) induces irreversible renal damage causing sustained elevation in blood pressure (BP) in Cyp1a1-Ren2 transgenic rats. In our current study we hypothesized that activation of the AT1-receptor (AT1R) ...

Abstract	Transient activation of the renin-angiotensin system (RAS) induces irreversible renal damage causing sustained elevation in blood pressure (BP) in Cyp1a1-Ren2 transgenic rats. In our current study we hypothesized that activation of the AT1-receptor (AT1R) leads to a T-cell response causing irreversible impairment of renal function and hypertension. Cyp1a1-Ren2 rats harbor a construct for activation of the RAS by indole-3-carbinol (I3C). Rats were fed a I3C diet between 4-8 weeks of age to induce hypertension. Next, I3C was withdrawn and rats were followed-up for another 12 weeks. Additional groups received losartan (20 mg/kg/day) or hydralazine (100 mg/kg/day) treatment between 4-8 weeks. Rats were placed for 24h in metabolic cages before determining BP at week 8, 12 and 20. At these ages, subsets of animals were sacrificed and the presence of kidney T-cell subpopulations was investigated by immunohistochemistry and molecular marker analysis. The development of sustained hypertension was completely prevented by losartan, whereas hydralazine only caused a partial decrease in BP. Markers of renal damage: KIM-1 and osteopontin were highly expressed in urine and kidney samples of I3C-treated rats, even until 20 weeks of age. Additionally, renal expression of regulatory-T cells (Tregs) was highly increased in I3C-treated rats, whereas the expression of T-helper 1 (Th1) cells demonstrated a strong decrease. Losartan prevented these effects completely, whereas hydralazine was unable to affect these changes. In young Cyp1a1-Ren2 rats AT1R activation leads to induction of an immune response, causing a shift from Th1-cells to Tregs, contributing to the development of irreversible renal damage and hypertension.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Hemodynamics/drug effects ; Hydralazine/pharmacology ; Hypertension/immunology ; Hypertension/metabolism ; Hypertension/pathology ; Hypertension/physiopathology ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Kidney/physiopathology ; Losartan/pharmacology ; Rats ; Rats, Transgenic ; Receptor, Angiotensin, Type 1/metabolism ; Renin-Angiotensin System/drug effects ; Renin-Angiotensin System/immunology ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; Time Factors
Chemical Substances	Biomarkers ; Receptor, Angiotensin, Type 1 ; Hydralazine (26NAK24LS8) ; Losartan (JMS50MPO89)
Language	English
Publishing date	2013-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0057815
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Article: Functional and structural postglomerular alterations in the kidney of prehypertensive spontaneously hypertensive rats.

Baumann, Marcus / van Essen, Helma / Hermans, J J Rob / Smits, Jos F M / Struijker-Boudier, Harry A J

Clinical and experimental hypertension (New York, N.Y. : 1993)

2005 Volume 26, Issue 7-8, Page(s) 663–672

Abstract: The kidney plays a major role in the development of hypertension. Following the Borst-Guyton theory of an altered set-point for fluid and electrolyte homeostasis we aim to investigate functional and structural renal parameter during the development of ... ...

Abstract	The kidney plays a major role in the development of hypertension. Following the Borst-Guyton theory of an altered set-point for fluid and electrolyte homeostasis we aim to investigate functional and structural renal parameter during the development of hypertension. Therefore we focus on counter current exchange related factors. We compared 4 and 8 weeks old Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) concerning basic renal parameters as creatinine and phosphorus clearance and urinary osmolality. Mean arterial pressure (MAP) was measured intra-arterially. Vasa recta were investigated using immunohistochemistry for alpha-smooth-muscle actin (ASMA) and plastification for geometric analyses. Blood pressure was not yet significantly elevated in SHR at 4 weeks but at 8 weeks it was higher in SHR (116+/-7 vs. 102+/-4 mm Hg; p<0.01). Kidney weight/body weight ratio was lower in SHR at both ages. In 4 weeks old SHR, phosphorus clearance and urinary osmolality were decreased compared to WKY [0.02+/-0.01 vs. 0.05+/-0.02 (ml/min* 100 g BW) p < 0.03; 14.2+/-2.2 vs. 18.9+/-2.9 (osmol/kg*24 h urine) p < 0.051 indicating reduced tubular reabsorption. At 8 weeks phosphorus clearance and urinary osmolality were comparable to WKY. alpha-Actin was found in vasa recta in a 4-times higher degree in SHR with a predominant location in the outer medulla. Radii of vasa recta in the outer medulla decreased during development. In plastificated sections vasa recta of SHR revealed sphincter-like pattern. Functional and structural alterations related to the counter current exchanger are already evident in prehypertensive SHR. During development of hypertension both factors get adapted to higher blood pressure level. Sphincter-like structures in vasa recta suggest contractility of pericytes/vascular smooth muscle cells (vSMC). As these were just seen in SHR that might allude to a higher potential to contract. We conclude that differences in postglomerular structure and function may contribute to the development of hypertension in SHR.
MeSH term(s)	Animals ; Blood Pressure/physiology ; Body Weight ; Creatinine/metabolism ; Hypertension, Renal/metabolism ; Hypertension, Renal/pathology ; Hypertension, Renal/physiopathology ; Kidney Glomerulus/blood supply ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Organ Size ; Phosphorus/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Renal Circulation/physiology ; Water-Electrolyte Balance/physiology
Chemical Substances	Phosphorus (27YLU75U4W) ; Creatinine (AYI8EX34EU)
Language	English
Publishing date	2005-02-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604757-9
ISSN	1064-1963 ; 0730-0077
ISSN	1064-1963 ; 0730-0077
DOI	10.1081/ceh-200031969
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Zs.A 1429: Show issues

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Article: Intrapericardial delivery enhances cardiac effects of sotalol and atenolol.

van Brakel, Thomas J / Hermans, J J Rob / Janssen, Ben J / van Essen, Helma / Botterhuis, Nicole / Smits, Jos F M / Maessen, Jos G

Journal of cardiovascular pharmacology

2004 Volume 44, Issue 1, Page(s) 50–56

Abstract: Targeting drugs to the heart by intrapericardial (i.p.c.) delivery may be a promising strategy to obtain higher drug efficiencies with lesser side effects. We examined whether i.p.c. delivery of sotalol and atenolol in rats offers advantages over ... ...

Abstract	Targeting drugs to the heart by intrapericardial (i.p.c.) delivery may be a promising strategy to obtain higher drug efficiencies with lesser side effects. We examined whether i.p.c. delivery of sotalol and atenolol in rats offers advantages over intravenous (i.v.) application. Following sustained IPC infusion of sotalol or atenolol, pericardial fluid levels exceeded plasma levels 97 and 134 times respectively (P < 0.01) resulting in 3.8 and 4.7 times higher overall left ventricular tissue drug levels (P < 0.05). In a second experiment, the effects of the i.p.c. or i.v. beta-blocker infusions on nitroprusside-induced tachycardia were studied in conscious rats. For both drugs, i.p.c. infusion of 0.03 mg/kg.h produced similar antitachycardiac effects as the 1 mg/kg.h i.v. dose. In a third set of studies, dP/dt max challenged by dobutamine infusion was assessed to study ventricular contractile function after i.v. and i.p.c. sotalol in anesthetized rats. i.p.c. sotalol infusion attenuated the dobutamine response curve to a greater extent than i.v. (P < 0.01). In conclusion, i.p.c. infusion of sotalol and atenolol results in high cardiac tissue concentrations with low systemic drug levels. Similar antitachycardiac effects can be obtained at a 10- to 30-fold lower dose compared with i.v. delivery. Also, depression of ventricular contractility is acquired at a substantially lower i.p.c. sotalol dose. Thus, beta-blocking properties of sotalol and atenolol can be greatly enhanced by applying them i.p.c.
MeSH term(s)	Adrenergic beta-Antagonists/administration & dosage ; Adrenergic beta-Antagonists/pharmacokinetics ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Atenolol/administration & dosage ; Atenolol/pharmacokinetics ; Atenolol/pharmacology ; Body Weight/drug effects ; Drug Delivery Systems ; Infusions, Intralesional ; Infusions, Intravenous ; Male ; Myocardial Contraction/drug effects ; Pericardium ; Rats ; Rats, Wistar ; Sotalol/administration & dosage ; Sotalol/pharmacokinetics ; Sotalol/pharmacology
Chemical Substances	Adrenergic beta-Antagonists ; Atenolol (50VV3VW0TI) ; Sotalol (A6D97U294I)
Language	English
Publishing date	2004-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/00005344-200407000-00007
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Article: Pharmacokinetic advantage of intrapericardially applied substances in the rat.

Hermans, J J Rob / van Essen, Helma / Struijker-Boudier, Harry A J / Johnson, Randolph M / Theeuwes, Felix / Smits, Jos F M

The Journal of pharmacology and experimental therapeutics

2002 Volume 301, Issue 2, Page(s) 672–678

Abstract: Intrapericardial application of therapeutic agents may open perspectives for target-directed therapy of the diseased heart. This study was performed to investigate whether intrapericardial drug application is beneficial from a pharmacokinetic point of ... ...

Abstract	Intrapericardial application of therapeutic agents may open perspectives for target-directed therapy of the diseased heart. This study was performed to investigate whether intrapericardial drug application is beneficial from a pharmacokinetic point of view. Male Wistar rats were provided with intrapericardial and intravascular catheters for substance administration and sampling. Intrapericardial bolus injections of fluorescent macromolecules [fluorescein isothiocyanate (FITC)-rat IgG, molecular weight about 155 kDa; Texas Red rat serum albumin, mol. wt. 67 kDa; Texas Red fibroblast growth factor (FGF), mol. wt. 18 kDa; and FITC heparin, mean mol. wt. 18 kDa] resulted in substance concentrations in pericardial fluid that exceeded those in plasma, for several hours. Pericardial fluid volumes of catheter-instrumented rats, derived from (initial) central compartment volumes, ranged between 0.5 and 0.9 ml/kg. After chronic (7 days) intrapericardial infusions with osmotic minipumps, pericardial fluid/plasma concentration ratios (local advantages) were 7 to 10 for the fluorescent proteins and >30 for FITC-heparin. This can be explained by the low substance clearances in pericardial fluid compared with plasma. Local advantages of the small substances cortisol (mol. wt. = 362.5) and a carbonic acid derivative thereof (mol. wt. = 348) were 14 and 420. Intrapericardial infusion of (125)I-FGF-2 yielded 8 times higher cardiac tissue levels than systemic infusion, whereas (125)I-FGF-2 was found in the entire heart. Pharmacokinetic profiles of intrapericardially applied substances are such that desired local drug concentrations can be obtained at lower dosages, whereas systemic concentrations remain low (thus reducing the potential risk of peripheral side effects). Therefore, intrapericardial application of therapeutic agents provides a promising strategy for site-specific treatment of heart or coronary diseases.
MeSH term(s)	Animals ; Autoradiography ; Drug Administration Routes ; Fibroblast Growth Factor 2/blood ; Fibroblast Growth Factor 2/pharmacokinetics ; Heparin/blood ; Heparin/pharmacokinetics ; Hydrocortisone/blood ; Hydrocortisone/pharmacokinetics ; Iodine Radioisotopes ; Male ; Models, Animal ; Myocardium/metabolism ; Pericardial Effusion/metabolism ; Pericardium/metabolism ; Rats ; Rats, Wistar
Chemical Substances	Iodine Radioisotopes ; Fibroblast Growth Factor 2 (103107-01-3) ; Heparin (9005-49-6) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2002-04-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.301.2.672
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Article: Determination of Aortic Elastic Modulus by Pulse Wave Velocity and Wall Tracking in a Rat Model of Aortic Stiffness

Marque, Valérie / van Essen, Helma / Struijker-Boudier, Harry A.J. / Atkinson, Jeffrey / Lartaud-Idjouadiene, Isabelle

Journal of Vascular Research

2001 Volume 38, Issue 6, Page(s) 546–550

Abstract: Several methods have been used to evaluate the elastic modulus of the aortic wall in the rat, but these have never been compared when used simultaneously. We measured thoracoabdominal pulse wave velocity (PWV) and changes in thoracic aorta diameter ... ...

Institution	Laboratoire de Pharmacologie Cardiovasculaire, EA3116, Faculté de Pharmacie, Université Henri Poincaré-Nancy 1, Nancy, France Department of Pharmacology and Toxicology, Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands
Abstract	Several methods have been used to evaluate the elastic modulus of the aortic wall in the rat, but these have never been compared when used simultaneously. We measured thoracoabdominal pulse wave velocity (PWV) and changes in thoracic aorta diameter during the cardiac cycle (with wall echo-tracking) in pentobarbital-anesthetized adult male Wistar rats; half of the group had previously received vitamin D3 plus nicotine (VDN) in order to increase the stiffness of the aortic wall. The Moens-Korteweg elastic modulus (EMK) was calculated from PWV and the ratio of the internal diameter to the medial thickness determined by histomorphometry following in situ pressurized fixation. The incremental elastic modulus (Einc) was calculated from the distensibility coefficient and end-diastolic diameter measured by wall echo-tracking and the medial thickness determined by histomorphometry. Both values were higher in VDN rats than in controls: Einc 8.9 ± 0.5 and 5.7 ± 0.4·106 dyne/cm2, p < 0.05; EMK 7.6 ± 0.5 and 4.1 ± 0.5·106 dyne/cm2, p < 0.05. Einc was greater than EMK and this was partially due to the fact that the in vivo end-diastolic diameter measured by ultrasound was greater than the mean aortic diameter measured ex vivo by histomorphometry. In conclusion, different methods for the measurement of the elastic properties of the aortic wall gave similar results in controls and in a rat model of aortic stiffness.
Keywords	Moens-Korteweg equation ; Histomorphometry ; Distensibility coefficient ; Medial thickness ; Thoracic aorta
Language	English
Publishing date	2001-12-07
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Research Paper
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000051090
Database	Karger publisher's database

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Zs.A 513: Show issues

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Article: Fadrozole reverses cardiac fibrosis in spontaneously hypertensive heart failure rats: discordant enantioselectivity versus reduction of plasma aldosterone.

Minnaard-Huiban, Monica / Emmen, Judith M A / Roumen, Luc / Beugels, Ilona P E / Cohuet, Géraldine M S / van Essen, Helma / Ruijters, Eveline / Pieterse, Koen / Hilbers, Peter A J / Ottenheijm, Harry C J / Plate, Ralf / de Gooyer, Marcel E / Smits, Jos F M / Hermans, J J Rob

Endocrinology

2008 Volume 149, Issue 1, Page(s) 28–31

Abstract: Reversal of cardiac fibrosis is a major determinant of the salutary effects of mineralocorticoid receptor antagonists in heart failure. Recently, R-fadrozole was coined as an aldosterone biosynthesis inhibitor, offering an appealing alternative to ... ...

Abstract	Reversal of cardiac fibrosis is a major determinant of the salutary effects of mineralocorticoid receptor antagonists in heart failure. Recently, R-fadrozole was coined as an aldosterone biosynthesis inhibitor, offering an appealing alternative to mineralocorticoid receptor antagonists to block aldosterone action. The present study aimed to evaluate the effects of R- and S-fadrozole on plasma aldosterone and urinary aldosterone excretion rate and to compare their effectiveness vs. the mineralocorticoid receptor antagonist potassium canrenoate to reverse established cardiac fibrosis. Male lean spontaneously hypertensive heart failure (SHHF) rats (40 wk) were treated for 8 wk by sc infusions of low (0.24 mg/kg.d) or high (1.2 mg/kg.d) doses of R- or S-fadrozole or by potassium canrenoate via drinking water (7.5 mg/kg.d). At the high dose, plasma aldosterone levels were decreased similarly by R- and S-fadrozole, whereas urinary aldosterone excretion rate was reduced only by S-fadrozole. In contrast, whereas at the high dose, R-fadrozole effectively reversed preexistent left ventricular interstitial fibrosis by 50% (vs. 42% for canrenoate), S-fadrozole was devoid of an antifibrotic effect. The low doses of the fadrozole enantiomers did not change cardiac fibrosis or plasma aldosterone but similarly reduced urinary aldosterone excretion rate. In conclusion, R-fadrozole may possess considerable therapeutic merit because of its potent antifibrotic actions in the heart. However, the observed discordance between the aldosterone-lowering and antifibrotic effects of the fadrozole enantiomers raises some doubt about the mechanism by which R-fadrozole diminishes cardiac collagen and about the generality of the concept of lowering aldosterone levels to treat the diseased heart.
MeSH term(s)	Aldosterone/blood ; Aldosterone/urine ; Animals ; Canrenoic Acid/pharmacology ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Collagen Type III/genetics ; Collagen Type III/metabolism ; Drug Evaluation, Preclinical ; Fadrozole/chemistry ; Fadrozole/therapeutic use ; Fibrosis ; Gene Expression Regulation/drug effects ; Heart/drug effects ; Heart Failure/prevention & control ; Heart Failure/urine ; Male ; Mineralocorticoid Receptor Antagonists/pharmacology ; Myocardium/metabolism ; Myocardium/pathology ; Rats ; Rats, Inbred SHR ; Stereoisomerism ; Structure-Activity Relationship ; Treatment Outcome
Chemical Substances	Collagen Type I ; Collagen Type III ; Mineralocorticoid Receptor Antagonists ; collagen type I, alpha 1 chain ; Aldosterone (4964P6T9RB) ; Canrenoic Acid (87UG89VA9K) ; Fadrozole (H3988M64PU)
Language	English
Publishing date	2008-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2007-0584
Database	MEDical Literature Analysis and Retrieval System OnLINE

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