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Biomedical subjects

A Januszewicz

Publications and source records attributed to A Januszewicz.

At least 55 records · Page 3Linked to original sources
PubMed1992

Effect of vasopressin and V1 receptors blockade on hypotensive action of ANP in normotensive (WKY) and spontaneously hypertensive rats.

The aim of the study was to find out whether vasopressin (AVP) modifies hypotensive and heart rate accelerating effects of atrial natriuretic peptide (ANP) in normotensive (WKY) and spontaneously hypertensive (SHR) conscious rats. The effect of i.v. administration of 1; 2 and 4 micrograms of ANP on blood pressure (MP) and heart rate (HR) was compared during i.v. infusion of 0.9% NaCl (NaCl), NaCl+AVP (1.2 ng kg-1 min-1) and NaCl+dEt2AVP (V1 receptors antagonist, 0.5 microgram kg-1 min-1). AVP increased MP in SHR and WKY and decreased HR in SHR. V1 antagonist decreased MP and increased HR only in SHR. In SHR ANP decreased MP and increased HR during NaCl, AVP and V1 antagonist infusion. In WKY these effects were observed only during AVP administration. In each experimental situation hypotension and tachycardia induced by ANP were greater in SHR than in WKY. In both strains ANP induced changes in MP and HR were enhanced during AVP in comparison to NaCl infusion. V1 antagonist did not modify effects of ANP in WKY and SHR. The results indicate that ANP abolishes hypertensive response induced by blood AVP elevation and that the basal levels of endogenous vasopressin acting through V1 receptors does not interfere with hypotensive action of ANP neither in WKY nor in SHR.

Animals↗
PubMed1992

[Primary arterial hypertension. Treatment with captopril and function of the left heart ventricle, concentration of catecholamine in blood and activity of renin].

We evaluated the effect of captopril treatment on left ventricular mass (LVM) and function in sustained mild-to-moderate primary hypertension. In 16 men aged 34.5 +/- 6.4 yrs. M-mode echo and pulsed wave Doppler recordings were obtained prior to and after 2 months captopril treatment (50-150 mg daily). No significant changes in heart rate, systolic blood pressure, ejection fraction, fractional shortening, cardiac output, LVM and Doppler-derived indices of mitral inflow were observed. Diastolic blood pressure measured during examination fell from 102.2 +/- 13.3 to 90.3 +/- 9 mmHg (p less than 0.026). No consistent correlations between catecholamines and indexes of left ventricular function were found. Two-month captopril therapy in mild-to-moderate hypertension results in diastolic blood pressure lowering with no effect on LVM or left ventricular function.

Adult↗
PubMed1991

[Atrial natriuretic peptide level in acute myocardial infarction].

Concentration of atrial natriuretic peptide (ANP) was studied in acute myocardial infarction (AMI), its association with ventricular arrhythmias (VA), left ventricular dysfunction and infarct size. Plasma ANP concentrations were measured at time: 0, 4, 8, 16, 24, 48 and 72 hours after admission in 11 patients (pts) with first AMI, up to 6 hours after the first symptoms. Ventricular arrhythmia was assessed by 24 hour Holter monitoring, left ventricular dysfunction by echocardiography and infarct size by serial CK-MB measurement in first 72 hours of AMI. In subsequent measurements the average plasma concentration of ANP (mean +/- SEM) was elevated: 42.2 +/- 9.9, 35.3 +/- 12.5, 33.9 +/- 8.3, 42.3 +/- 8.3, 36.9 +/- 6.4, 60.7 +/- 9.3, 47.8 +/- 12.0 fmol/ml. The maximal plasma ANP concentration was significantly higher (p less than 0.01) in 4 pts with VA 4th grade acc. to Lown than in 7 pts without VA (102.6 +/- 17.9 vs 41.1 +/- 6.4). The maximal level of ANP--153.3 fmol/ml in a patient with paroxysmal supraventricular tachycardia was observed. There were no significant correlations between plasma ANP and infarct size, size of left atrium and contractility disturbances of left ventricle.

Adult↗
PubMed1990

[Effects of 4-hour erect posture and furosemide on the blood level of atrial natriuretic peptide in patients with primary arterial hypertension].

The arterial pressure, the pulse frequency, the concentration of arterial natriuretic peptide (ANP), the aldosterone++ concentration and the plasma renin activity were determined in patients with primary hypertension after administration of furosemide in conditions of active assuming of erect position. The ANP concentration was lowered in that conditions both in the patients and in healthy subjects.

Adult↗
PubMed1990

[Free serotonin level in the blood of patients with borderline and essential hypertension].

Serotonin appears to play an important part in the pathogenesis of essential hypertension. Various studies have shown, that the metabolism of serotonin may be disturbed in some pathological conditions for example in hypertension. It concerns also the changed mechanisms of uptake and release of serotonin. The certain blood vessels may become more hypersensitive to the vasoconstrictor effects of serotonin in patients with hypertension than in normal subjects. During chronic treatment with ketanserin, S2-serotonergic antagonist, blood pressure is reduced in spontaneously hypertensive rats and in humans. This fact can also indicate indirectly, that that serotonin plays a part in the pathogenesis of essential hypertension. The aim of the study was to determine the concentration of free serotonin (S) in the blood of 15 patients with sustained essential hypertension in the mean age 32.8 +/- 1.8, of 23 patients with borderline essential hypertension in the mean age 29.0 +/- 3.0 and of 10 normal subjects in the mean age 31.1 +/- 1.7 years. Plasma free serotonin was determined by fluorometric method. All patients and controls were investigated at the hospital. They were on normosodium diet, without drugs for last two weeks. The fasting blood samples were collected in the supine position. Free serotonin blood concentration was significantly higher in hypertensive group than in normal subjects. The important difference of serotonin blood concentration between two groups of hypertensive patients was noticed. It was significantly higher in group of patients with sustained hypertension, than in group with borderline hypertension (p less than 0.05). Our results are similar to the observations of other authors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of physical exercise on atrial natriuretic factor and plasma catecholamine concentrations in patients with essential uncomplicated hypertension.

Plasma atrial natriuretic factor (ANF) and catecholamine concentrations were determined in 11 untreated patients with uncomplicated essential hypertension and seven normotensive subjects during graded submaximal exercise on a treadmill (loads: I 40%, II 60%, III 80% of maximal oxygen consumption). No significant differences in plasma ANF and catecholamine concentrations were found between the hypertensive and the normotensive subjects. The results do not support the presence of significant differences in the release of ANF and catecholamines during dynamic exercise between patients with uncomplicated essential hypertension and normotensive subjects.

Adult↗
PubMed1989

[Atrial natriuretic peptide in patients with primary arterial hypertension].

Atrial natriuretic peptide (ANP) activity was studied in 33 males with borderline and established essential hypertension. No significant differences of serum ANP concentration were stated in patients with borderline and established uncomplicated hypertension in comparison with the control group.

Adolescent↗
PubMed1989

[Correlations of atrial natriuretic peptide and catecholamine levels in the blood during surgical removal of pheochromocytoma].

Atrial natriuretic peptide concentrations (ANP) were determined in 4 patients with pheochromocytoma during its surgical removal. There was no correlation among ANP level, plasma catecholamines concentrations and blood pressure. Increase of plasma ANP concentration after tumor removal can be explained by simultaneously observed hypervolemia. It proves that ANP secretion mostly depends on enlarged central blood volume.

Adrenal Gland Neoplasms↗
PubMed1988

Atrial natriuretic factor enhances vasopressin-induced bradycardia in normotensive (WKY) but not in spontaneously hypertensive (SHR) rats.

Effect of elevation of blood atrial natriuretic peptide (rat 1-28 ANF) level on pressor responses and bradycardia elicited by vasopressin (AVP) was compared in conscious normotensive (WKY) and spontaneously hypertensive (SHR) rats 14-16 weeks old, instrumented with arterial and venous catheters 1-2 days prior to the experiment. Blood pressure and heart rate were determined before and after i.v. injection of 2.5, 5.0 and 10.0 ng of AVP under control conditions (infusion of saline) and during infusion of ANF at a rate of 0.3 micrograms kg-1 min-1. Administration of ANF did not influence pressor responsiveness to AVP (determined as a maximum increase of systolic blood pressure) neither in WKY nor in SHR, however, it elongated the pressor response to the lowest dose of AVP in WKY. Atrial natriuretic factor significantly enhanced bradycardic responsiveness to AVP (determined as a maximum decrease of HR) in WKY but not in SHR. Reduction of heart rate in relation to the corresponding elevation of the systolic pressure (delta HR/delta SP) was also significantly greater in WKY but not in SHR. This effect was significant when blood pressure increases elicited by AVP did not exceed 40 mmHg. The results suggest that ANF potentiates reflex bradycardia elicited by AVP. This action may be a mechanism buffering blood pressure increases in response to AVP. Absence of this effect in SHR may be related to the impairment of the reflex control of blood pressure in this strain.

Animals↗
PubMed1986

Atriopeptin III does not alter cardiac performance in rats.

The effects of atriopeptin III (APIII) on systemic haemodynamics were examined in 12 anaesthetized rats. Five minutes following intravenous injection (i.v.) of 10 micrograms/kg APIII, cardiac output CO, measured by electromagnetic flowmetry, stroke volume and mean arterial pressure (MAP) decreased by 14, 13 and 8% (P less than 0.05), respectively, and total peripheral resistance (TPR) increased by 10% (P less than 0.05). Heart rate (HR) and left ventricular end-diastolic pressure (LVEDP) did not change. In order to examine cardiac performance, whole blood was infused into three groups of 12 rats each receiving either no injection, APIII (10 micrograms/kg i.v.) or APIII (10 micrograms/kg i.v.) plus a continuous infusion of phenylephrine to increase MAP to pre-injection levels. Cardiac performance curves did not differ among the three groups. These data indicate that the immediate decreases in MAP and CO produced in rats by a maximum natriuretic bolus dose of APIII were not mediated by a negative myocardial inotropic effect.

Animals↗
PubMed1986

Conversion factors of high- to low-molecular-weight forms of atrial natriuretic factor.

The atrial natriuretic factor (ANF) is comprised of a 126-amino-acid precursor (pro-ANF) and its biologically active fragments. Partially purified pro-ANF and its larger fragments (greater than 10,000 daltons) have been referred to as high-molecular-weight (Mr) ANF, the partially purified smaller fragments (less than 10,000 daltons) as low Mr ANF. In vitro, mild proteolysis of high Mr ANF yielded low Mr ANF and enhanced biological activity. In the rat, pro-ANF was the predominant atrial form; however, low Mr ANF was largely released from isolated perfused hearts, which suggests that conversion of pro-ANF to low Mr ANF occurred immediately before or during secretion. High Mr ANF was also found in the perfusate of isolated rat hearts and in the plasma of rats, which suggests that some pro-ANF was secreted with low Mr ANF. Evidence for extraatrial conversion and activation of pro-ANF comes from two studies. 1) Intra-renal-arterial injection of high Mr ANF had little renal vascular action, whereas its i.v. injection caused renal vascular dilation, which suggests that the renal vasodilatory action of high Mr ANF became activated during circulation. 2) When high Mr ANF was incubated with rat blood or rat platelets in vitro, its natriuretic activity was converted to low Mr ANF within minutes; the platelet-induced conversion was associated with enhanced activity in relaxing aortic smooth muscle.

Animals↗