Skip header and navigation

Refine By

33 records – page 1 of 4.

Adrenomedullin gene expression in the rat heart is stimulated by acute pressure overload: blunted effect in experimental hypertension.

https://arctichealth.org/en/permalink/ahliterature54511
Source
Endocrinology. 1997 Jun;138(6):2636-9
Publication Type
Article
Date
Jun-1997
Author
H. Romppanen
M. Marttila
J. Magga
O. Vuolteenaho
P. Kinnunen
I. Szokodi
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Endocrinology. 1997 Jun;138(6):2636-9
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Animals
Argipressin - pharmacology
Atrial Natriuretic Factor - biosynthesis
Blood Pressure - drug effects
Heart - physiology - physiopathology
Heart Failure, Congestive - metabolism
Heart Ventricles
Humans
Hypertension - metabolism - physiopathology
Male
Myocardium - metabolism
Natriuretic Peptide, Brain
Peptide Biosynthesis
Peptides
RNA, Messenger - biosynthesis
Rats
Rats, Inbred Strains
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Time Factors
Transcription, Genetic - drug effects
Abstract
The levels of adrenomedullin (ADM), a newly discovered vasodilating and natriuretic peptide, are elevated in plasma and ventricular myocardium in human congestive heart failure suggesting that cardiac synthesis may contribute to the plasma concentrations of ADM. To examine the time course of induction and mechanisms regulating cardiac ADM gene expression, we determined the effect of acute and short-term cardiac overload on ventricular ADM mRNA and immunoreactive ADM (ir-ADM) levels in conscious rats. Acute pressure overload was produced by infusion of arginine8-vasopressin (AVP, 0.05 microg/kg/min, i.v.) for 2 h into 12-week-old hypertensive TGR(mREN-2)27 rats and normotensive Sprague-Dawley (SD) rats. Hypertension and marked left ventricular hypertrophy were associated with 2.2-times higher ir-ADM levels in the left ventricular epicardial layer (178 +/- 36 vs. 81 +/- 23 fmol/g, P
PubMed ID
9165059 View in PubMed
Less detail

Blood pressure, plasma atrial natriuretic peptide and catecholamines during rapid ventricular pacing and effects of beta-adrenergic blockade in coronary artery disease.

https://arctichealth.org/en/permalink/ahliterature11920
Source
Am J Cardiol. 1992 Jan 1;69(1):35-9
Publication Type
Article
Date
Jan-1-1992
Author
K J Peuhkurinen
H V Huikuri
H. Ruskoaho
J T Takkunen
Author Affiliation
Department of Internal Medicine, Oulu University Central Hospital, Finland.
Source
Am J Cardiol. 1992 Jan 1;69(1):35-9
Date
Jan-1-1992
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Atrial Natriuretic Factor - blood
Blood Pressure - drug effects
Cardiac Pacing, Artificial
Catecholamines - blood
Coronary Disease - blood - drug therapy - physiopathology - therapy
Epinephrine - blood
Female
Humans
Male
Middle Aged
Norepinephrine - blood
Propranolol - therapeutic use
Regression Analysis
Research Support, Non-U.S. Gov't
Time Factors
Abstract
To study neurohumoral control mechanisms of the hemodynamic response to ventricular tachycardia, arterial blood pressure, plasma atrial natriuretic peptide (ANP) and catecholamine levels were monitored during simulated ventricular tachycardia before and after administration of beta blockade. Tachycardia was simulated by ventricular pacing at 150 beats/min for 150 seconds in 9 patients without and 14 with angiographically demonstrable coronary artery disease (CAD). The effects of intravenous propranolol (0.15 mg/kg) were evaluated in 7 control subjects and in 13 patients with CAD. Arterial blood pressure decreased to its minimum within 5 seconds after onset of pacing in all patients, the decrease being 27 and 30% (p = not significant) in the groups without and with CAD, respectively. Propranolol did not affect the initial decline, but blunted subsequent recovery. The ANP baseline levels were similar in both groups, increasing by 60% (p less than 0.05) and 71% (p less than 0.02) in the groups without and with CAD, respectively, during ventricular pacing. After administration of propranolol the increase in ANP was 180% in both groups. Rapid ventricular pacing did not affect catecholamine levels before propranolol, but after propranolol norepinephrine increased by 71 (p less than 0.02) and 97% (p less than 0.01) in patients without and with CAD, respectively. There was a significant correlation (r = 0.53, p = 0.001) between pacing-induced ANP and norepinephrine changes, but changes in arterial blood pressure did not correlate with those in either of these hormones. Thus, beta-adrenergic blockade blunts blood pressure recovery during simulated ventricular tachycardia. However, this is partly counterbalanced by increased circulating norepinephrine levels.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed ID
1530902 View in PubMed
Less detail

Brain natriuretic peptide in plasma, atria, and ventricles of vasopressin- and phenylephrine-infused conscious rats.

https://arctichealth.org/en/permalink/ahliterature11547
Source
Endocrinology. 1994 Jun;134(6):2505-15
Publication Type
Article
Date
Jun-1994
Author
J. Magga
M. Marttila
P. Mäntymaa
O. Vuolteenaho
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology and Physiology, University of Oulu, Finland.
Source
Endocrinology. 1994 Jun;134(6):2505-15
Date
Jun-1994
Language
English
Publication Type
Article
Keywords
Animals
Argipressin - pharmacology
Heart Atria - metabolism
Heart Ventricles - metabolism
Hypertension - metabolism
Male
Myocardium - metabolism
Natriuretic Peptide, Brain
Nerve Tissue Proteins - blood - genetics - metabolism
Phenylephrine - pharmacology
RNA, Messenger - metabolism
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Research Support, Non-U.S. Gov't
Abstract
To evaluate the mechanisms of brain natriuretic peptide (BNP) gene expression, we determined the effect of acute cardiac overload (from 30 min to 4 h) on atrial and ventricular BNP mRNA levels in normal and hypertrophied myocardium. Arginine8 vasopressin (AVP; 0.05 microgram/kg.min) and l-phenylephrine (PHE; 20 micrograms/kg.min) were infused iv to increase cardiac workload in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. At the age of 10-22 months, during the established phase of ventricular hypertrophy, baseline BNP synthesis was increased in the hypertrophic ventricular cells of SHR, as reflected by about 2-fold (P
PubMed ID
8194476 View in PubMed
Less detail

B-type natriuretic peptide: a myocyte-specific marker for characterizing load-induced alterations in cardiac gene expression.

https://arctichealth.org/en/permalink/ahliterature33626
Source
Ann Med. 1998 Aug;30 Suppl 1:39-45
Publication Type
Article
Date
Aug-1998
Author
J. Magga
O. Vuolteenaho
H. Tokola
M. Marttila
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Ann Med. 1998 Aug;30 Suppl 1:39-45
Date
Aug-1998
Language
English
Publication Type
Article
Keywords
Adult
Animals
Cardiac Volume - physiology
Cells, Cultured
Child, Preschool
Comparative Study
Dogs
Gene Expression
Genetic Markers - physiology
Guanylate Cyclase - genetics - metabolism
Humans
Hypertrophy, Left Ventricular - physiopathology
Mice
Mice, Transgenic
Myocardium - cytology - metabolism
Rats
Receptors, Atrial Natriuretic Factor - genetics - metabolism
Research Support, Non-U.S. Gov't
Sensitivity and specificity
Swine
Abstract
Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide are the known members of the mammalian natriuretic peptide system. ANP and BNP genes are expressed in a specific manner in cardiac myocytes. They are natriuretic and diuretic hormones and cause vasorelaxation. ANP is mainly synthesized in the atria of the normal adult heart. However, ventricular hypertrophy is characterized by an augmentation of the synthesis and release of ANP from the ventricles. BNP is expressed in both the atria and the ventricles, but is mainly released from the ventricles. The major determinant of ANP and BNP secretion is wall stretch, and the levels of BNP messenger RNA increase substantially in response to cardiac overload. Acute increase in BNP gene expression occurs within 1 h and mimics the rapid induction of proto-oncogenes in response to haemodynamic stress. BNP can be used as a myocyte-specific marker to identify mechanisms that couple acute mechanical overload to alterations in cardiac gene expression.
PubMed ID
9800882 View in PubMed
Less detail

cAMP- and cGMP-independent stretch-induced changes in the contraction of rat atrium.

https://arctichealth.org/en/permalink/ahliterature10288
Source
Pflugers Arch. 2000 Nov;441(1):65-8
Publication Type
Article
Date
Nov-2000
Author
P. Tavi
M. Weckström
H. Ruskoaho
Author Affiliation
Department of Physiology, University of Oulu, Finland. pasi.tavi@oulu.fi
Source
Pflugers Arch. 2000 Nov;441(1):65-8
Date
Nov-2000
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Animals
Atrial Function
Biomechanics
Calcium - metabolism
Cyclic AMP - metabolism
Cyclic GMP - metabolism
Isoproterenol - pharmacology
Male
Mechanoreceptors - physiology
Myocardial Contraction - drug effects - physiology
Rats
Rats, Sprague-Dawley
Abstract
The stretch-induced changes in contraction force, cAMP and cGMP in isolated rat left atrium were studied. Increasing the diastolic intra-atrial pressure from 1 cmH2O to 8 cmH2O caused an immediate (
PubMed ID
11205063 View in PubMed
Less detail

Differential regulation of cardiac adrenomedullin and natriuretic peptide gene expression by AT1 receptor antagonism and ACE inhibition in normotensive and hypertensive rats.

https://arctichealth.org/en/permalink/ahliterature54153
Source
J Hypertens. 1999 Nov;17(11):1543-52
Publication Type
Article
Date
Nov-1999
Author
J. Magga
J. Kalliovalkama
H. Romppanen
O. Vuolteenaho
I. Pörsti
M. Kähönen
J P Tolvanen
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
J Hypertens. 1999 Nov;17(11):1543-52
Date
Nov-1999
Language
English
Publication Type
Article
Keywords
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals
Atrial Natriuretic Factor - genetics
Blood Pressure - drug effects
Cardiomegaly - pathology
Enalapril - pharmacology
Gene Expression - drug effects
Heart - physiopathology
Hypertension - genetics - physiopathology
Losartan - pharmacology
Male
Natriuretic Peptide, Brain
Peptides - genetics
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Receptors, Angiotensin - antagonists & inhibitors
Reference Values
Research Support, Non-U.S. Gov't
Abstract
OBJECTIVE: To study the effects of long-term treatment with the type 1 angiotensin (AT1) receptor antagonist losartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril, on cardiac adrenomedullin (ADM), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) gene expression. METHODS: Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were given losartan (15 mg/kg per day) or enalapril (4 mg/kg per day) orally for 10 weeks. The effects of drugs on systolic blood pressure, cardiac hypertrophy, ANP, BNP and ADM mRNA and immunoreactive-ANP (IR)-ANP, IR-BNP and IR-ADM levels in the left ventricle and atria were compared. RESULTS: Losartan and enalapril treatments completely inhibited the increase of systolic blood pressure occurring with ageing in SHR. The ratio of heart to body weight was reduced in both losartan- and enalapril-treated SHR and WKY rats. Treatment with losartan or enalapril reduced left ventricular ANP mRNA and IR-ANP in both strains, and ventricular BNP mRNA levels in SHR rats. Inhibition of ACE, AT1 receptor antagonism, changes in blood pressure or cardiac mass had no effect on left ventricular ADM gene expression in SHR and WKY rats. In addition, atrial IR-ANP and IR-ADM levels increased in SHR whereas IR-BNP levels decreased in WKY and SHR rats in response to drug treatments. CONCLUSIONS: Our results show that ventricular ADM synthesis is an insensitive marker of changes in haemodynamic load or cardiac hypertrophy. Furthermore, the expression of ADM, ANP and BNP genes is differently regulated both in the left ventricle and atria in response to AT1 receptor antagonism and ACE inhibition.
PubMed ID
10608466 View in PubMed
Less detail

The effect of aminophylline on right heart function in young pigs after ligation of the right coronary artery.

https://arctichealth.org/en/permalink/ahliterature54098
Source
Pharmacol Toxicol. 2000 Apr;86(4):192-6
Publication Type
Article
Date
Apr-2000
Author
M B Spalding
T I Ala-Kokko
K. Kiviluoma
H. Ruskoaho
S. Alahuhta
Author Affiliation
Department of Anaesthesiology, University Hospital of Oulu, Finland. spami@sun3.oulu.fi
Source
Pharmacol Toxicol. 2000 Apr;86(4):192-6
Date
Apr-2000
Language
English
Publication Type
Article
Keywords
Aminophylline - pharmacology
Animals
Blood Pressure - drug effects
Cardiotonic Agents - pharmacology
Coronary Vessels - drug effects - physiopathology - surgery
Disease Models, Animal
Dose-Response Relationship, Drug
Female
Heart - drug effects - physiopathology
Heart Rate - drug effects
Heart Ventricles - drug effects - pathology - physiopathology
Hemodynamic Processes - drug effects
Ligation - adverse effects
Male
Myocardial Infarction - etiology - pathology - physiopathology
Stroke Volume - drug effects
Swine
Vascular Resistance - drug effects
Abstract
An experimental model of right heart failure was developed to determine the effects of fluid loading and aminophylline on right heart function. We hypothesised that aminophylline would specifically improve right heart function through a decrease in pulmonary vascular resistance and, possibly, an increase in cardiac contractility. Right heart infarct was induced in ten experimental pigs and seven control pigs by ligating branches of the right coronary artery. The effect of fluid loading with a colloid solution and subsequent bolus doses of aminophylline on haemodynamics was observed. Fluid loading improved haemodynamics as expected. Aminophylline transiently improved cardiac index and pulmonary vascular resistance, but simultaneously caused an increase in heart rate and a decrease in stroke volume. Although aminophylline may reduce right heart afterload, it did not improve overall cardiac function in this experimental model of right heart infarction.
PubMed ID
10815753 View in PubMed
Less detail

Effect of atenolol and pindolol on the phorbol ester-induced coronary vasoconstriction in the isolated perfused heart of the rat.

https://arctichealth.org/en/permalink/ahliterature12471
Source
Br J Pharmacol. 1988 Jun;94(2):573-83
Publication Type
Article
Date
Jun-1988
Author
H. Ruskoaho
Author Affiliation
Department of Pharmacology, University of Oulu, Finland.
Source
Br J Pharmacol. 1988 Jun;94(2):573-83
Date
Jun-1988
Language
English
Publication Type
Article
Keywords
Animals
Atenolol - pharmacology
Coronary Vessels - drug effects
Heart - drug effects
In Vitro
Male
Perfusion
Phorbol Esters - pharmacology
Pindolol - pharmacology
Rats
Rats, Inbred Strains
Receptors, Adrenergic, beta - drug effects - physiology
Vasoconstriction - drug effects
Abstract
1. The effects of atenolol (beta 1-adrenoceptor antagonist without partial agonistic activity) and pindolol (beta 1- and beta 2-antagonist with partial agonistic activity) were studied on basal coronary vascular tone and on the phorbol ester-induced coronary vasoconstriction in the rat perfused heart. 2. The addition of the phorbol ester 12-0-tetradecanoyl-phorbol-13-acetate (TPA; 1.8 X 10(-8)-1.6 X 10(-7) M) into the perfusion fluid during perfusion of rat heart at constant flow caused a dose-dependent, sustained increase in perfusion pressure. The vasoconstrictor response in hearts of reserpine-treated rats to infusion of TPA was similar to that of non-reserpine treated hearts. 3. Infusion of a calcium channel agonist Bay K 8644 at a concentration of 4 X 10(-7) M enhanced, whereas isoprenaline (1 X 10(-5) M), dibuturyl-cyclic AMP (1.6 X 10(-4) M) and forskolin (1 X 10(-6) M), which elevate intracellular concentrations of cyclic AMP, all inhibited the coronary vasoconstriction induced by TPA. 4. Pindolol, in doses which produced comparable inhibition of isoprenaline-induced tachycardia, dose-dependently attenuated the phorbol ester-induced increase in perfusion pressure, whereas atenolol had no effect. The inhibitory action of pindolol (2 X 10(-5) M) on TPA-induced vasoconstriction was blocked by addition of 2.2 X 10(-5) M propranolol into the perfusion fluid. When infused alone, atenolol (2 X 10(-4) M) significantly increased coronary vascular tone, but pindolol had no effect. 5. The present results indicate that pindolol has coronary vasodilator properties due to stimulation of vascular beta-adrenoceptors. If stenosis dilatation of coronary artery spasm is an important component of the anti-anginal effect of beta-blocking drugs, the possession of partial agonistic property by a beta-blocking drug may be of importance in maintaining coronary flow.
PubMed ID
2840163 View in PubMed
Less detail

Effect of endurance training on atrial natriuretic peptide gene expression in normal and hypertrophied hearts.

https://arctichealth.org/en/permalink/ahliterature54920
Source
J Appl Physiol. 1994 Mar;76(3):1184-94
Publication Type
Article
Date
Mar-1994
Author
P. Mäntymaa
J. Arokoski
I. Pörsti
M. Perhonen
P. Arvola
H J Helminen
T E Takala
J. Leppäluoto
H. Ruskoaho
Author Affiliation
Department of Pharmacology, University of Oulu, Finland.
Source
J Appl Physiol. 1994 Mar;76(3):1184-94
Date
Mar-1994
Language
English
Publication Type
Article
Keywords
Animals
Atrial Natriuretic Factor - biosynthesis - genetics - immunology
Blotting, Northern
Body Weight - physiology
Cardiomegaly - metabolism
Dogs
Eating - physiology
Female
Lactates - blood
Lactic Acid
Male
Myocardium - metabolism
Organ Size - physiology
Physical Conditioning, Animal
Physical Endurance - physiology
RNA, Messenger - biosynthesis
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Rats, Wistar
Research Support, Non-U.S. Gov't
Abstract
We studied the effects of physical endurance training on atrial natriuretic peptide (ANP) gene expression in beagle dogs, Wistar rats, and spontaneously hypertensive rats (SHR). The dogs underwent a gradually increased running training up to 40 km/day on a treadmill for 55 wk while the nontrained sibling control dogs were kept in their cages throughout the study. Endurance training caused a significant 13% (P
PubMed ID
8005862 View in PubMed
Less detail

Effect of phorbol ester on the release of atrial natriuretic peptide from the hypertrophied rat myocardium.

https://arctichealth.org/en/permalink/ahliterature55275
Source
Br J Pharmacol. 1991 Feb;102(2):453-61
Publication Type
Article
Date
Feb-1991
Author
P. Kinnunen
T. Taskinen
M. Järvinen
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Br J Pharmacol. 1991 Feb;102(2):453-61
Date
Feb-1991
Language
English
Publication Type
Article
Keywords
Animals
Atrial Natriuretic Factor - genetics - secretion
Cardiomegaly - genetics - physiopathology
Gene Expression
Heart - drug effects - physiology
Hemodynamic Processes - drug effects
In Vitro
Male
Perfusion
RNA, Messenger - genetics - metabolism
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Research Support, Non-U.S. Gov't
Tetradecanoylphorbol Acetate - pharmacology
Abstract
1. To determine the cellular mechanisms of atrial natriuretic peptide (ANP) release from ventricular cardiomyocytes, the secretory and the cardiac effects of a phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), known to stimulate protein kinase C activity in heart cells, were studied in isolated, perfused heart preparations from 2- and 21-month-old Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. TPA was added to the perfusion fluid for 30 min at a concentration of 46 nM after removal of atrial tissue. Additionally, atrial and ventricular levels of immunoreactive ANP (IR-ANP) and ANP mRNA, the distribution of ANP within ventricles as well as the relative contribution of atria and ventricles in the release of ANP were studied. 2. Ventricular hypertrophy that gradually developed in hypertensive rats resulted in remarkable augmentation of ANP gene expression, as reflected by elevated levels of immunoreactive ANP and ANP mRNA. The total amount of IR-ANP in the ventricles of the SHR rats increased 41 fold and ANP mRNA levels 12.9 fold from the age of 2 to 21 months. At the age of 21 months, levels of IR-ANP and ANP mRNA in the ventricles of SHR rats were 5.4 fold and 3.7 fold higher, respectively, than in the normotensive WKY rats. Immunohistochemical studies demonstrated ANP granules within the hypertrophic ventricles of the old SHR rats, but not within normal ventricular tissue. 3. In isolated perfused heart preparations, the severely hypertrophied ventricular tissue of SHR rats after atrialectomy secreted more ANP into the perfusate than did the control hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed ID
1826618 View in PubMed
Less detail

33 records – page 1 of 4.