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Biomedical subjects

A Brattström

Publications and source records attributed to A Brattström.

At least 19 recordsLinked to original sources
PubMed1994

Effects of central angiotensin II and angiotensin III on baroreflex regulation.

In the present study the cardiovascular effects of intracerebroventricularly (i.c.v.) applied angiotensin II (AN II) and angiotensin III (AN III) were analysed in conscious Wistar rats. The baroreceptor heart reflex (BHR) was elicited by intravenous bolus injection of both phenylephrine (1 microgram) and sodium nitroprusside (5 micrograms) before and after i.c.v. administration (1.5 and 15 min) of the peptides. Administration of 20 ng and 200 ng AN II produced a short increase in inter-beat interval (IBI) and a long-lasting increase in mean blood pressure (MBP), inclusive of a drinking response. Only after the high dose of 200 ng AN II we found a continuous impairment in the BHR for reflex bradycardia. Inversely, the small doses of both 100 pg AN II and 100 pg AN III were without effects on IBI and MBP; they induced an enhancement in BHR for the reflex bradycardia and after 100 pg AN II it was also found for the reflex tachycardia. Pretreatment with 20 nmol amastatin (AM), a specified aminopeptidase A inhibitor, followed by 100 pg An II suppressed the enhancement in BHR. AM alone was without effects in this respect. These findings suggest that: 1) the influence of central angiotensin on the BHR could be dose-dependent in the opposite way and 2) AN III seems to be the active form and involved in the central blood pressure regulatory mechanism.

Angiotensin II↗
PubMed1993

Effects of central substance P on baroreflex regulation.

The effects of intracerebroventricularly (i.c.v.) administered Substance P (100 pg, 1 microgram, 10 micrograms) on mean blood pressure (MBP), inter-beat interval (IBI) and the baroreceptor heart reflex (BHR) were studied in conscious Wistar rats. The BHR was induced by intravenous injection of both phenylephrine (1 microgram) and sodium nitroprusside (5 micrograms) before and after SP administration (3 and 15 min). The dose of 100 pg SP was without effect on the resting values of both MBP and IBI but enhanced the BHR sensitivity by about + 0.5 ms/mm Hg in the phenylephrine test 3 min after i.c.v. SP. 1 microgram and 10 micrograms SP caused a long-lasting dose dependent increase in MBP and changed the IBI. In contrast to the results obtained with 100 pg, the BHR sensitivity was impaired-1 microgram SP: -0.2 ms/mm Hg (phenylephrine) and -0.45 ms/mm Hg (nitroprusside), 10 micrograms SP: -0.35 ms/mm Hg (phenylephrine). These changes in BHR sensitivity were only recognised 3 min, but not 15 min, after i.c.v. treatment even hough changes in the resting values of MBP and IBI were still present at 15 min. These data suggest that SP through the cerebrospinal fluid may participate in central cardiovascular control and, moreover, it may influence the baroreflex regulation.

Animals↗
PubMed1992

Central substance P increased blood pressure, heart rate and splanchnic nerve activity in anaesthetized rats without impairment of the baroreflex regulation.

In anaesthetized rats the baroreflex was checked before and 15 min after i.c.v. administration of 10 micrograms SP. The baroreflex was checked indirectly by relating both the reflex prolongation in heart period (inter-beat-interval: IBI) and the reflex inhibition of SNA to a pharmacologically induced BP rise. After i.c.v. administration of SP (n = 10) the resting values of the BP increased significantly from 73 +/- 16 mm Hg to 86 +/- 9 mm Hg (diastolic pressure) and from 98 +/- 20 mm Hg to 113 +/- 14 mm Hg (systolic pressure) whilst in the control group (n = 14) the BP remained constant (63 +/- 9 vs 63 +/- 7 mm Hg diastolic pressure and 106 +/- 12 vs 106 +/- 9 mm Hg systolic pressure). In the experimental group the resting value in IBI was shortened significantly from 218 +/- 40 ms to 167 +/- 28 ms (controls: 218 +/- 22 ms vs 218 +/- 18 ms) and the SNA (estimated in arbitrary units) rose significantly by about 50% in relation to the reference period before i.c.v. SP (3.31 +/- 0.11 vs 6.27 +/- 0.17 arbitrary units per IBI). In contrast, the baroreflex behaved similarly before and after any treatment, i.e. both the reflex prolongation in IBI (1.34 +/- 0.75 vs 1.39 +/- 0.95 ms/mm Hg) and the reflex inhibition of SNA (0.0312 +/- 0.01 vs 0.0555 +/- 0.015 arbitrary units/mm Hg) caused by that pharmacologically induced BP rise were comparable before and after i.c.v. SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1992

Neuropeptides within the nucleus tractus solitarii modulate the central cardiovascular control process.

Local administration of small amounts of vasopressin, angiotensin or endothelin into the nucleus tractus solitarii elicits similar decreases in blood pressure and heart rate. These central effects oppose the peripheral action of these hormones on the cardiovascular system. The baroreceptor-heart-reflex, however, is influenced differentially: vasopressin and angiotensin II enhances the sensitivity of the reflex but angiotensin III impairs it. In this way the cardiovascular system may be adjusted to different demands including those related to electrolyte and fluid homeostasis.

Angiotensin II↗
PubMed1992

Cardiovascular responses to centrally applied sodium chloride solution.

In conscious and anaesthetized rats the baroreceptor heart reflex (BHR) was checked before and after i.c.v. application of isotonic or hypertonic (0.6 M; 1.0 M) NaCl solution, artificial cerebrospinal fluid (aCSF) and 1.0 M mannitol solution. The BHR was tested by evaluating the alteration of the inter-beat interval (IBI) in response to an artificial BP rise or drop which had been evoked by i.v. bolus injection of either phenylephrine or sodium nitroprusside. The slope of the correlation function was taken to index the reflex sensitivity. In anaesthetized rats the mean sensitivity of the BHR was 0.6 ms/mm Hg (phenylephrine). l.c.v. administration of isotonic NaCl solution did not change BP, IBI or the BHR sensitivity, whilst i.c.v. infusion of hypertonic NaCl solution increased BP and shortened IBI. The BHR sensitivity was impaired only when 1.0 M NaCl solution was i.c.v. infused by 0.23 ms/mm Hg. In conscious rats the mean sensitivity of the BHR was 1.14 ms/mm Hg (phenylephrine) and 1.35 ms/mm Hg (sodium nitroprusside). In the conscious rats i.c.v. bolus injection of hypertonic NaCl solution increased BP as in anaesthetized rats, however, the IBI was prolonged, whilst 1.0 M mannitol solution and aCSF were without any influence on BP, IBI and BHR. l.c.v. administration of hypertonic NaCl solution reduced the BHR sensitivity by approximately 0.6 ms/mm Hg.

Anesthesia↗
PubMed1991

Intracerebroventricular administration of hypertonic sodium chloride solution reduces the sensitivity of the baroreceptor heart reflex in anaesthetized rats.

Intracerebroventricular (i.c.v.) infusion of hypertonic sodium chloride solution increased blood pressure (BP) and shortened heart period (interbeat-interval: IBI) that is why an impairment in baroreflex regulation is believed to be part of that process. Therefore, in anaesthetized rats (1.35 g urethane/kg BW) the baroreceptor-heart reflex (BHR) was tested before and during i.c.v. infusion (15 min) of isotonic or hypertonic (0.6 M, 1.0 M) sodium chloride solution by inducing an acute BP rise by i.v. pressoric agents (phenylephrine, methoxamine). The evoked reflex prolongation of the IBI was taken to estimate the sensitivity of that BHR (delta ms/mm Hg). Whilst i.c.v. infusion of isotonic sodium chloride solution did not affect BHR sensitivity, hypertonic sodium chloride solution not only elevated BP and shortened IBI but also reset and impaired the BHR. Therefore, an increased central sensitivity to sodium chloride might not only increase BP but also impair the buffering capacity of the BHR against this rise and in this way support development of hypertension.

Anesthesia↗
PubMed1990

Central vasopressin impairs the baroreceptor heart rate reflex in conscious rats.

In conscious, unrestrained rats, the resting values of mean arterial blood pressure (BP) and heart rate (HR) as well as the baroreceptor heart rate reflex (BHR) were measured before and after intracerebroventricular (i.c.v.) application of arginine vasopressin (AVP). The BHR was induced by intravenous (i.v.) injection of different doses of phenylephrine. Basal values of BP and HR were 114 +/- 2.4 mm Hg and 376 +/- 13 beats/min (mean +/- SE). These values were not altered by i.c.v. application of vehicle or 5, 10, 30, 300, 3,000 pg AVP or 1 pg AVP antagonist [(D(CH2)5Tyr(Me)-AVP)]. Ten and 30 pg AVP administered i.c.v. attenuated the phenylephrine-induced decrease in HR. Lower or higher doses of AVP were not effective. Administration of the AVP antagonist i.c.v. sensitized the BHR. When the BHR was rechecked 24 h after treatment, the influence of the i.c.v.-administered peptides had disappeared. We conclude that AVP through the cerebrospinal fluid impairs the baroreflex regulation.

Animals↗
PubMed1990

Cardiovascular effects of vasopressin micro-injections into the nucleus tractus solitarii in normotensive and hypertensive rats.

In anesthetized, normotensive Wistar rats, Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), 100 pg [Arg8]-vasopressin was micro-injected bilaterally into the nucleus tractus solitarii (NTS). Blood pressure and the interbeat heart interval were measured. In both Wistar rats and WKY the interbeat interval was prolonged and blood pressure was decreased, while in SHR only the interbeat interval was prolonged. Thus, within a very low dose range, the influence of [Arg8]-vasopressin within the NTS on mechanisms of cardiovascular regulation seems to differ between normotensive rats and SHR.

Animals↗
PubMed1989

Vasopressin, vasopressin fragments and a C-terminal peptide of the vasopressin precursor share cardiovascular effects when microinjected into the nucleus tractus solitarii.

Arginine-vasopressin (VP), the VP fragments VP-(1-8), [pGlu4,Cyt6]VP-(4-9) and -(4-8), and a fragment of the C-terminal glycopeptide of the VP precursor [CPP-(22-39)] decreased blood pressure and heart rate in anesthetized rats when microinjected bilaterally into the nucleus tractus solitarii (NTS). The magnitude of the effect was similar at doses of 20 pg, except for VP-(1-8) which required about 500 pg. The strongest decrease in blood pressure and heart rate was observed with 100 pg VP. Higher doses of other peptides either were ineffective [CPP-(22-39)] or increased blood pressure [( pGlu4,Cyt6]VP-(4-9) and -(4-8)). VP metabolites thus may participate in the control of cardiovascular functions exerted by VP. The effect of CPP-(22-39) indicates that the C-terminal glycopeptide of the VP precursor contains biological activity, which may support the cardiovascular action of VP in the NTS.

Animals↗
PubMed1988

Vasopressin micro-injections into the nucleus tractus solitarii decrease heart rate and blood pressure in anaesthetized rats.

Bilateral micro-injections of arginine vasopressin into the nucleus tractus solitarii caused a dose-dependent (1-100 pg) decrease in blood pressure and heart rate in anaesthetized rats. Higher doses (1-20 ng) caused an increase in both parameters. Subcutaneous injection of an antagonist [d(CH2)5Tyr(Me)-arginine vasopressin] failed to block these effects. Micro-injections of the antagonist (0:1-100 pg) into the nucleus tractus solitarii decreased blood pressure and the heart rate similarly to arginine vasopressin. The effect of the antagonist disappeared after about 30 min. At that time administration of arginine vasopressin into the nucleus tractus solitarii was ineffective in inducing changes in blood pressure and the heart rate. When a low-dose (0.1 or 1 pg) antagonist was used the effect of 100 pg arginine vasopressin was partially inhibited. We conclude that administration of arginine vasopressin into the nucleus tractus solitarii is effective at low doses, and may be involved in inhibitory cardiovascular control at the level of nucleus tractus solitarii.

Animals↗
PubMed1988

[Long-term hypotensive effects of substance P on the stress induced hypertension of primates].

The Substance P (SP) level in blood is lower in hypertensive individuals than in normotensive ones. Intravenous application of SP leaves the normotensive blood pressure largely unaffected, but decreases the enhanced blood pressure. Further studies on the effect of SP (i.v. application of 2.5 micrograms/kg b.w.) were performed on 26 primates; the results were as follows: With normotensive primates SP no effect on blood pressure. Upon repeated chasing and subsequent immobilization (load) the animals developed an arterial hypertension. Under the same load, the animals failed to develop hypertension if they were treated with SP 1 h before. A load-induced hypertension could be interrupted by injection of SP even after 3 weeks following initial load; the after-controls one year later revealed normotensive blood pressure values. Application of SP with two other animal groups with a manifest hypertonus lowered the blood pressure only transitorily. It is concluded that i.v. application of SP can prevent the development of stress-induced hypertension and, with existing manifest hypertension, leads to reduced blood pressure only transitorily. An indirect action with peripheral site of attack is assumed.

Animals↗
PubMed1986

Blood pressure response to intravenous noradrenaline is influenced by substance P in normotensive and hypertensive rabbits.

Substance P (SP) applied to the cerebral ventricles elevates arterial blood pressure (BP). This elevation is mediated by an increased sympathetic tone and, moreover, could be attenuated by intravenous (i.v.) SP. To check the assumption that a change of adrenoceptor efficiency might contribute to the attenuation, SP (5 ng/kg per min) was continuously given i.v. and 20 micrograms SP injected intracerebroventricularly (i.c.v.) in anaesthetized normotensive as well as hypertensive rabbits. The BP response to 5 micrograms noradrenaline (NA) was checked within a control period before SP was given and rechecked 30 min after i.c.v. SP with continued i.v. infusion. Under these circumstances SP altered the BP response to NA qualitatively and quantitatively. An initial BP drop was followed by a rise which was remarkably smaller in magnitude than that obtained within the control period. The BP response to phenylephrine (PHE), however, was not altered by the identical SP protocol. Substance P application only i.v. or only i.c.v. was ineffective. Moreover, no differences could be revealed between normotensive and hypertensive animals in the BP response to NA. It is concluded that the beta-adrenoceptor efficiency changed similarly in the normotensive and hypertensive rabbits with i.v. SP, provided sympathetic tone had previously increased. In this manner i.v. SP might modify an exaggerated sympathetic tone which might be implicated in the pathogenesis of arterial hypertension.

Animals↗
PubMed1984

[Long-term effects of substance P on the higher nervous activity of primates].

The conditioned reflex, blood pressure and behavioral parameters prior to and during a single application of Substance P to unnarcotized primates were tested on four successive days, as well as of physiological saline also administered as a single application on four successive days. The evaluations were done each after 24 h from application. In a dose range from 0.25-25 micrograms/kg b.wt. the drug improved the performance of the conditioned reflex, while at 250 micrograms/kg b.wt. no improvement was ascertainable. At high doses behavioral disorders occurred. Blood pressure values showed no detectable reactions. From 25 micrograms/kg b.wt. onwards the application produced distinct immediate vegetative reactions which, however, subsided still during the 4-day procedure. At 250 micrograms/kg b. wt., the vegetative reactions became increasingly stronger. It is concluded that the individual functional circuits of the organism respond differently to Substance P. Behavioral reactions occurring 24 h after the application were not considered to be direct effects of Substance P. It is assumed that Substance P gives a push to other neuroactive systems.

Animals↗
PubMed1984

[Aortic baroreceptor function in narcotized rabbits during alpha-adrenoceptor blockade with prazosin].

Since alpha-adrenoceptor blockade alters the mechanical vessel wall properties, the arterial baroreceptor function is to be changed also by this type of blockade. In 13 rabbits narcotized with chloralose and urethan, therefore, the aortic baroreceptor function was tested together with the baroreceptor heart reflex prior to and after intravenous administration of prazosin (0.005, 0.01, 0.05 mg per kg BW). By inflation and respective deflation of a balloon catheter lying with its tip in the thoracal aorta the arterial blood pressure level ahead was changed over a range as much as 30 to 50 mm Hg. The arterial blood pressure in the aortic arch, the heart rate and the electroneurogram from the peripheral stump of the left aortic nerve were registered. Intravenous administration of prazosin slowed down the arterial blood pressure in a dose related manner, and the heart rate remained similar. After having applied any doses of prazosin the baroreceptor heart reflex was completely abolished. The baroreceptor sensitivity was remarkably increased by prazosin. The characteristic curve describing the baroreceptor function was shifted to the left and was steeper. It was concluded that the baroreceptor heart reflex is directly blocked by the action of prazosin against the transmission in the parasympathetic pathway, and, mediated by the influence of prazosin on the vessel wall properties, the arterial baroreceptor becomes more sensitive.

Animals↗
PubMed1981

Coincidental relationship of activity in the sympathetic ganglioglomerular nerve innervating the carotid bifurcation with the intracarotid systolic pulses.

The innervation of the carotid bifurcation by the ganglioglomerular nerve originating from the superior cervical ganglion has brought about the idea that the baroreceptor function is under efferent control. Provided that the efferent activity coincides with the systolic pulse, the receptor elements may be influenced at this critical moment. Therefore, the coincidental relationship was investigated between the efferent sympathetic bursts of the ganglioglomerular nerve and the intracarotid systolic pressure rise. It was found that the bursts appear regularly before pressure rises and continue for the ensuing 160-220 msec. The bursts onset varied greatly depending on the R-R interval. On the contrary, the burst cessation occurred with a constant delay following systolic pressure rise. The single burst duration was found to be modulated by the rhythm of respiration and altered by hemorrhage, but the coincidence remained consistent. It is, therefore, concluded that the temporal prerequisite exists which enables the baroreceptor to be influenced by sympathetic control just at the moment when systolic pulse affects the carotid baroreceptor.

Animals↗
PubMed1981

Modification of carotid baroreceptor function by electrical stimulation of the ganglioglomerular nerve.

The effect of ganglioglomerular nerve (GN) stimulation on canine carotid baroreceptors has been investigated. In the first group of experiments, a reflex response of the mean arterial blood pressure (MAP) was observed, MAP decreased during GN stimulation. The time-course and magnitude of the pressure decrease were dependent upon the stimulus frequency. In a second experimental group, isolated carotid bifurcations were continuously perfused with arterial blood (at constant flow rate) and changes in the perfusion pressure were used as an indicator of vessel wall reaction to GN stimulation. The vessel wall response began 15-20 sec after onset of the stimulation and a steady-state level was reached again after about 100 sec of stimulation. In a third group of experiments, the carotid baroreflex was investigated during periods with and without stimulation of the GN. During GN stimulation the magnitude of reflex responses was reduced, the working range of the baroreceptors displaced and the input-output relationship shifted towards lower intrasinus pressure values. From these findings it is concluded that efferent sympathetic activity (ESA) in the GN supplying the carotid bifurcation, affects the baroreceptor reaction in two ways: (i) by a short-lasting increase in baroreceptor sensitivity due to their direct influence; and (ii) by a more sustained and much slower-acting mechanism mediated by vessel wall stiffness (compliance) change (indirect influence).

Animals↗