Overall Cardiovascular Regulation

ÖBerg, Bengt

doi:10.1146/annurev.ph.38.030176.002541

Cited by 57 publications

(21 citation statements)

References 122 publications

(206 reference statements)

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“…In agreement with the present findings and in agreement with other studies in which conclusions about the sympathetic outflow were drawn from effector organ responses (for references see Korner, 1971;Sleight, 1974;Oberg, 1976;Kirchheim, 1976) Levison, Barnett & Jackson, 1966;Gero & Gerova, 1967;Stegemann & Tibes, 1969;Angell James & Daly, 1970;Schmidt, Kumada & Sagawa, 1972 (Resnicoff, Harris, Hampsey & Schwartz, 1969;Ninomiya et al 1971;Kendrick, Oberg & Wennergren, 1972;Wallin et al 1974;Wallin et al 1975) Wallin (1977) showed that in a given subject the mean burst incidence was remarkably constant in different muscle nerves, not only in one recording but also when recordings were repeated with intervals of weeks or months. This lack of correlation between the static blood pressure level and the 'level' of MSA in face of an intimate relationship between transient variations in blood pressure and sympathetic activity suggests that the sympathetic outflow to the vascular bed of skeletal muscle is of importance for buffering acute blood pressure changes but has little influence on the long term blood pressure level.…”

Section: Discussionsupporting

confidence: 94%

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Sundlöf

Wallin

1978

The Journal of Physiology

550

507

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SUMMARY1. Recordings of multi-unit sympathetic activity were made from median or peroneal muscle nerve fascicles in thirty-three healthy subjects, resting in recumbent position. Simultaneous recordings of intra-arterial blood pressure were made in seventeen subjects. The neural activity, quantified by counting the number of pulse synchronous sympathetic bursts in the mean voltage neurogram (burst incidence), was plotted against the arterial blood pressure level and the age of the subjects. The effects of spontaneous temporary blood pressure fluctuations were studied by correlating different pressure parameters of individual heart beats to the probability of occurrence of a sympathetic burst and to the amplitude of the occurring burst.2. Between different subjects there were marked differences in burst incidence, from less than 10 to more than 90 bursts/100 heart beats. No correlation was found to interindividual differences in the arterial blood pressure level but there was a slight tendency for increasing burst incidence with increasing age.3. Irrespective of the magnitude of the burst incidence, the bursts always occurred more frequently during spontaneous transient blood pressure reductions than during transient increases in blood pressure. When, for each heart cycle, the occurrence of a sympathetic burst was correlated with different blood pressure parameters there was regularly a close negative correlation to diastolic pressure, a low correlation to systolic and an intermediary negative correlation to mean blood pressure. There was a positive correlation to pulse pressure and to pulse interval.4. When measured for individual heart beats, not only the occurrence but also the mean voltage amplitude of the sympathetic bursts tended to increase with decreasing diastolic pressure.5. In a given subject when comparing heart beats with the same diastolic pressure, the occurrence as well as the amplitude of the sympathetic bursts was higher for heart beats occurring during falling than for heart beats occurring during rising blood pressure. For a given change in diastolic blood pressure, sympathetic activity changed more if pressure was falling than if it was rising.6. The findings suggest that the sympathetic outflow is modulated by arterial baroreflex mechanisms and that transient variations in the strength of the activity are, to a large extent, determined by diastolic blood pressure fluctuations. The intimate correlation with 'dynamic' variations in blood pressure and the absence of correlation to the 'static' blood pressure level suggests that the sympathetic outflow 6. SUNDLJF AND B. G. WALLIN to skeletal muscles is of importance for buffering acute blood pressure changes but has little influence on the long term blood pressure level. The difference in reflex sensitivity between falling and rising pressure indicates that acute blood pressure decreases may be buffered more efficiently than acute blood pressure increases.7. In twenty-seven subjects baroreflex latency was calculated from the QRScomplexes in the e...

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Section: Discussionsupporting

confidence: 94%

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Sundlöf

Wallin

1978

The Journal of Physiology

550

507

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“…On the other hand, it may be less sensitive to the baroreceptor evoked sympathoinhibition. What evidence there is would not support this latter hypothesis (see Oberg, 1976). Finally in this respect, intravenous administration of 5-HT2 antagonists characteristically increase femoral arterial conductance in anaesthetized cats (Ramage, 1985;1988) and IVth ventricular application of the 5-HT2 antagonist cinanserin in the present experimental system (Shepheard et al, 1990) caused an increase in femoral arterial conductance.…”

Section: Discussionmentioning

confidence: 60%

Investigation of the effects of IVth ventricular administration of the 5‐HT₂ agonist, 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI), on autonomic outflow in the anaesthetized cat

Shepheard¹,

Jordan

Ramage³

1991

British J Pharmacology

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1 The effects of IVth ventricular injections of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on renal, splanchnic and cardiac sympathetic nerve activities, phrenic nerve activity, arterial blood pressure, heart rate, femoral arterial conductance, tracheal and intragastric pressures were investigated in achloralose anaesthetized, neuromuscular blocked and artificially ventilated cats. 2 Cumulative doses of DOI (80, 160 and 320nmolkg-1) injected into the IWth ventricle caused an increase in mean arterial blood pressure, a fall in femoral arterial conductance, an increase in tracheal pressure and a decrease in the rate of phrenic nerve bursts but did not affect any of the other variables recorded. 3 Even after i.v. administration of the peripheral 5-HT2 antagonist BW501C67 (2 mg kg-1) following the highest dose of DOI there was still a significant pressor response, a fall in femoral arterial conductance and small increase in tracheal pressure. 4 In control experiments, intravenous infusion of noradrenaline to raise blood pressure to the levels obtained during the cumulative doses of DOI caused large falls in renal, splanchnic and cardiac nerve activities which were all significantly lower than those recorded during the cumulative doses of DOI. 5 The results of this study provide evidence for a brainstem site of action of DOI in producing hypertension and further support the hypothesis that central 5-HT2 receptors are involved in the control of skeletal muscle and skin vascular beds.

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“…21 Because nisoldipine did not have an appreciable effect on neurally evoked vasoconstriction and pressure elevation in the present study, the mechanism responsible for the hypotensive effect of nisoldipine in the conscious animals is not clear. One possibility that could reconcile this inconsistency is that nisoldipine might lower resting sympathetic nerve activity by an effect on the discharge rate of vasomotor neurons within the central nervous system.…”

Section: Neural Vasoconstrictionmentioning

confidence: 59%

Selective antagonism of humoral versus neural vasoconstrictor responses by nisoldipine.

Lappe

Barron²,

Faber

et al. 1985

Hypertension

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SUMMARY The effects of nisoldipine administration on vascular reactivity to humoral and neural vasoconstrictor stimuli were examined in the intact rat. For these experiments, rats were instrumented with miniaturized pulsed Doppler flow probes to allow continuous measurement of renal, mesenteric, and hindquarters blood flow. In conscious and anesthetized rats, intravenous doses of angiotensin II (75 and 150 ng/kg), norepinephrine (0.6 and 1.2 /xg/kg), and epinephrine (0.6 and 1.2 /zg/kg) caused dose-dependent increases in arterial pressure and renal and mesenteric vascular resistance. Nisoldipine (0.7 /xg/min) administration significantly attentuated (p < 0.05) the pressor and regional vasoconstrictor actions of all three circulating pressor agents; however, nisoldipine infusion had little effect on neurally mediated regional vasoconstrictor responses elicited by electrical stimulation of the posterior hypothalamus or greater splanchnic nerve. These data indicate that nisoldipine depressed vascular responsiveness to humoral vasoconstrictor agents, while neural vasoconstrictor responses were unaffected. Thus nisoldipine appears to exert preferential antagonistic effects on humoral rather than on neural vasoconstrictor stimuli. (Hypertension 7: 216-222, 1985) KEY WORDS • calcium entry blockers • norepinephrine • epinephrine • angiotensin II neural vasoconstriction • vascular reactivity • regional vascular resistance T HE second-generation dihydropyridine calcium entry blocker (CEB) nisoldipine 1 has been demonstrated to lower arterial pressure by reducing total peripheral resistance in experimental animals 2 " 5 and hypertensive patients. Several investigators have suggested that, in addition to direct smooth muscle relaxation, 2 6 7 nisoldipine may lower arterial pressure, in part, by noncompetitively antagonizing aadrenergic receptor vasoconstrictor responses. Nisoldipine and other CEBs have been reported to selectively antagonize ctj-adrenergic receptor mediated vasoconstriction in isolated smooth muscle 6 -8 and in pithed rats and cats.9 "" These effects may depend on the specific tissue or animal species being studied, however; other investigators have reported that CEBs attenuate both a,-and a 2 -adrenergic vasoconstriction. Supported by grants HLB-14388 and HLB-07121 from the National Heart, Lung and Blood Institute, National Institutes of Health, and a gift from the Searle Family Trust.Address for reprints: Dr. Michael J. Brody, Department of Pharmacology, University of Iowa College of Medicine, Iowa City, Iowa 52242.Received March 12, 1983; revision accepted September 19, 1984. receptor responses, CEBs appear to inhibit angiotensin II (ANG II) vasoconstrictor responses in the isolated perfused hindquarters of the dog 16 and the pithed rat. 17The effects of CEBs on vascular reactivity to pressor stimuli in intact animals, however, are relatively unknown.In a previous study in our laboratory, 4 using a pulsed Doppler flowmeter to monitor regional blood flow, we described the effects of nisoldipine on ...

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Overall Cardiovascular Regulation

Cited by 57 publications

References 122 publications

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Investigation of the effects of IVth ventricular administration of the 5‐HT₂ agonist, 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI), on autonomic outflow in the anaesthetized cat

Selective antagonism of humoral versus neural vasoconstrictor responses by nisoldipine.

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Overall Cardiovascular Regulation

Cited by 57 publications

References 122 publications

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age

Investigation of the effects of IVth ventricular administration of the 5‐HT2 agonist, 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI), on autonomic outflow in the anaesthetized cat

Selective antagonism of humoral versus neural vasoconstrictor responses by nisoldipine.

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Investigation of the effects of IVth ventricular administration of the 5‐HT₂ agonist, 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI), on autonomic outflow in the anaesthetized cat