摘要:

SUMMARY1Rapid resetting of the arterial baroreceptor threshold in the normal circulation extends the pressure range over which baroreflexes operate at high gain. During sustained falls and rises in resting blood pressure (BP), changes in reflex threshold may be greater or less than those of the receptors, through interactions with other sources of afferent drive (e.g. cardiac baroreceptors). In chronic hypertension the magnitude of the reflex resetting again corresponds to that of the arterial baroreceptors, probably because of the resetting of the threshold of the cardiac receptors.2.‘Baroreflexes’in intact animals are compound reflexes with input from both arterial and non‐arterial baroreceptors (e.g. cardiac/pulmonary baroreceptors). The steady‐state responses can be characterized by BP‐autonomic output function curves, which are often sigmoidal, with a well‐defined effector response range and gain. Both sets of input contribute to the high gain component close to resting, with the arterial baroreceptors the major source of reflex drive; the non‐arterial baroreceptors also contribute over this part of the reflex and their role increases considerably at high and low BP.3In chronic mild/moderate hypertension the changes in baroreflex properties are similar to those of moderate acute rises in BP or in cardiac load; heart rate range of the vagal component of the cardiac baroreflex is depressed, gain is slightly enhanced and the Valsalva‐total peripheral resistance (TPR) reflex is unaltered. In severe hypertension: (i) vagal heart rate range and gain are further depressed; and (ii) there is depression of the Valsalva‐TPR reflex, much as observed in constrictor reflexes during acute hypertension in normal animals. Circulatory disturbances produce engagement of non‐arterial baroreceptors more readily in hypertensives than in normotensives; depression of baroreflexes in hypertension is due partly to enhanced drive from these receptors and partly due to reduction in the gain of the arterial baroreceptors.4The reflex vagal depression and that of neural constrictor reflexes can be considered as important homeostatic mechanisms that limit the effects of circulatory perturbations on cardiac filling pressures and on excessive rises in

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb02995.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1. The pharmacology and ionic regulation of [3H]‐2‐d‐2‐amino‐5‐phosphonopentanoic acid ([3H]‐d‐AP5) and [3H]‐dl‐2‐amino‐7‐phosphonoheptanoic acid ([3H]‐dl‐AP7) binding to homogenates of rat cerebral cortex were examined using radioligand binding methodology.2. Both [3H]‐d‐AP5 and [3H]‐dl‐AP7 labelled a single population of binding sites with dissociation constants of 0.39 and 1.8 μmol/l, respectively. The density of binding sites found with [3H]‐dl‐AP7 was 13 times greater than that found with [3H]‐d‐AP5.3. The ionic requirements of the [3H]‐d‐AP5 binding site in the presence of chloride were such that calcium acetate enhanced binding, while magnesium and sodium acetate both decreased binding. In the absence of chloride both calcium and chloride ions stimulated binding.4. In a chloride‐free buffer calcium acetate stimulated binding of [3H]‐dl‐AP7 in a biphasic manner. Chloride ions (ammonium salt) enhanced binding slightly at low concentrations (0.1–1.0 mmol/l) above which binding was reduced to non‐specific levels. The ionic dependence of [3H]‐dl‐AP7 binding had some similarities to the previously defined GLU‐C site.5. The pharmacological profile of the site labelled by [3H]‐d‐AP5 was consistent with that of a recognition site forN‐methyl‐d‐aspartate (NMDA) as defined in electrophysiological experiments. [3H]‐dl‐AP7 did not label an NMDA site as several non‐NMDA ligands displaced binding with high affinity and the binding was not stereospecific as found for [3H]‐d‐AP5. Moreover, the pharmacological profile of the [3H]‐d

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb01908.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1. Acute hormonal and renal effects of dilevalol (200 mg), a non‐selective β‐blocking drug with vasodilator properties, were compared with placebo in six normal men on constant sodium intake.2. Control and treatment blood pressures were lower with dilevalol than placebo, although the pattern of blood pressure fall was similar in both.3. Plasma active renin and aldosterone concentrations were lower on dilevalol than placebo after 4 h of recumbency (P<0.05).4. Total plasma renin, renin substrate, cortisol and atrial natriuretic peptide concentrations were similar on dilevalol and placebo.5. There were no differences in glomerular filtration rate and no deleterious biochemical or haematological changes on dilevalol or pla

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb01909.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1The article reviews the phenylephrine‘ramp’method for studying the baroreceptor‐heart rate reflex and the method of power spectral analysis for studying variability of blood pressure and of the R‐R interval.2These methods have been used to study changes in reflex properties during arousal from sleep, changes which occur acutely after physical exercise and with training, changes in hypertension, and after myocardial infarction.3Several of the above changes are attributable to altered properties of the arterial baroreceptors, but some involve changes in central nervous information pro

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb02996.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1We examined whether or not circulating alpha‐agonist modified baroreflex vasoconstriction of the hindlimb, using anaesthetized dogs in which the limb was vascularly isolated and perfused with blood from a donor dog using a pulsatile pump.2The open‐loop gain (G) of the baroreflex was estimated from changes in mean arterial pressure following mild quick haemorrhage from the aorta of the recipient dog.3The hindlimb perfusion pressure increased after haemorrhage due to neurogenic vasoconstriction.4An overall gain (Gh) of the baroreflex hindlimb vascular bed control system was estimated from the ratio of the increase in hindlimb perfusion pressure to the change in systemic arterial pressure of the recipient dog.5Administration of a relatively selective ai‐agonist with no prejunctional P2 stimulating action (phenylephrine) or a selective a2‐agonist (clonidine) to the donor dog increased its systemic arterial pressure and augmented Gh.6Since both drugs were administered to the donor dog and could not enter into the recipient dog, these drugs did not affect the recipient's sympathetic nervous system, including the central nervous system and afferent limb of the baroreflex system. Therefore, these drugs could modify baroreflex vasoconstriction of the hindlimb only at the junction of the efferent sympathetic nerve and the vascular smooth muscle.7It was concluded that postjunctional a‐adrenoceptor stimulation augments neurogenic vasocon

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb02997.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1Cardiac baroreflex sensitivity (BRS) and its sympathetic and vagal components were studied after atropine and propranolol administrations in conscious genetically hypertensive (LH), normotensive (LN) and low blood pressure (LL) rats of the Lyon strain at 5, 9, 13 and 70 weeks of age.2LH rats older than 9 weeks exhibit a lower BRS than age‐matched LN and LL controls.3The vagal component of cardiac baroreflex is predominant. In LN rats, this component increases up to 9 weeks of age.4The sympathetic component of cardiac baroreflex is small and identical in the three strains and does not alter with age.5Thus, in normotensive rats, the increase in BRS during maturation reflects mainly the vagal component. The development of hypertension prevents this physiological increase in the sensitivity of the vagal component of cardiac baroreflex leading to a reduced BR

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb02998.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1The age‐related changes in mean arterial pressure (MAP), heart rate (HR), and baroreflex sensitivity (BRS) were studied in spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats from 4 to 20 weeks of age.2Intra‐arterial blood pressure (BP) was continuously recorded for 24 h in conscious, freely moving rats. Twenty‐four hour MAP and HR were calculated by an online computer. Baroreflex sensitivity was measured by phenylephrine infusion.3In SHR, BRS was significantly lower than in WKY as early as 4‐5 weeks, at which time MAP in SHR was only slightly raised. During subsequent weeks, rapid increase in MAP occurred in SHR, in association with progressive bradycardia.4It was concluded that a reduced BRS may be detected in young prehypertensive SHR and this impairment of BRS may be central

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb02999.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1To investigate whether cardiopulmonary baroreflex control contributes to the pathogenesis and progression of hypertension, we have evaluated the function of the cardiopulmonary baroreflex in 22 patients with essential hypertension and in 17 volunteers with normotension. The normotensi ve group consisted of 8 subjects with a family history of hypertension and nine with no family history.2Forearm vascular resistance (FVR) and central venous pressure (CVP) were measured under control conditions when – 10 mmHg lower body negative pressure was applied; the cardiopulmonary slope (CPS = AFVR/ACVP) was calculated as an index of the cardiopulmonary baroreflex function.3CPS was significantly higher in hypertensives (6.0±3.93 [s.d.], P<0.01 and also tended to be higher in normotensives with a family history of hypertension (3.9±3.53, P<0.05), compared with normotensives without a family history of hypertension (1.7±0.88).4When the hypertensives were divided into two groups, depending on whether CPS was greater or less than 6.0 units, cardiac wall thickness (20 ± 1.6 mm vs 23 ± 3.2 mm, P<0.05) and the renal vascular resistance (20.9 ± 6.52 units vs 28.9 ± 7.32 units, P<0.05) were both significantly higher in the Low CPS group.5These findings suggest that cardiopulmonary baroreflex function was augmented even in normotensive subjects with hypertensive relatives, as compared with those without hypertensive subjects. Furthermore, cardiopulmonary baroreflex function was augmented in the early stages of hypertension and diminished further with increasing

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb03000.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1The baroreflex‐mediated changes in plasma norepinephrine (NE) and heart period (RR interval) to phenylephrine (PE)‐evoked pressor and nitroprusside (NP)‐evoked depressor stimulations were studied in 19 patients with chronic essential hypertension, 12 with borderline hypertension and in 11 age‐matched normal controls.2Intravenous infusion of PE at a rate of 0.25‐1.0 |ig/kg/min induced dose‐related increases in fhean arterial pressure (MAP) and in RR interval and a decrease in plasma NE. Similarly, NP infusion at a rate of 0.1‐0.4 ug/kg/min evoked the opposite changes in each variable. The reflex sensitivity was defined as the slope of linear regression between the changes in RR interval and MAP (RR/MAP) and between those in plasma NE (% of the baselines) and MAP (%NE/MAP).3Both RR/MAP and %NE/MAP for pressor and depressor stimulations were reduced below values found in normal subjects, in both chronic and borderline hypertensives.4The values of %NE/MAP was negatively related to the basal plasma NE during falls in blood pressure(r=‐0.401,P<0.05).5The %NE/MAP may be a useful index of the sympathetic component of baro‐reflex sensitivity. A decrease in %NE/MAP in hypertensive and borderline hypertensive patients suggests a blunted sensitivity of the sympathetic con

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb03001.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

SUMMARY1Two strains of rabbits have been bred with marked differences in their cardiac baroreflex sensitivity (BRS). The difference in cardiac BRS was attenuated by naloxone. We compared the sympathetic responses to a pressor stimulus in these two strains, by measuring the changes in plasma catecholamines in the presence and absence of naloxone.2Cardiac BRS was assessed in eight rabbits of each group by the steady‐state method. Two weeks later, both ear arteries and one ear vein were cannulated. Mean arterial pressure (MAP) and heart rate (HR) were recorded from one artery and blood samples (5 mL) for plasma catecholamines (CA) taken before, and during the peak of the pressor response to intravenous phenylephrine (PE, 20 ug/kg) from the other. The experiment was repeated 2‐3 weeks later in rabbits with high BRS (Group I) after injection of naloxone 0.1 mg/kg, i.v.3Resting MAP and HR did not differ in the two groups. The mean gains of the cardiac baroreflex were 23.3 ± 2.2 ms/mmHg in Group I and 6.3 ± 1.1 ms/mmHg in Group II. After PE, MAP rose by 54.5 ± 1.8 mmHg in Group II and 40.3 ± 3.6 mmHg in Group I(P<0.02). The pressor response was associated with a 31 % reduction in plasma noradrenaline (NA) in Group I and a 34% increase in Group II. The reduction in NA was significantly correlated with the degree of bradycardia in Group I (r = 0.72, P<0.05) and with BRS in both groups (r = 0.78,P<0.01). Naloxone reduced BRS in Group I to 8.2 ± 1.0 ms/mmHg and virtually abolished the fall in plasma NA in response to PE.4We suggest that stimulation of cardiopulmonary afferents by a strong pressor stimulus in Group I rabbits results in sympathetic inhibition which involves the mediation of opioid

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1989.tb03002.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY