Announcing the ‘Ulf von Euler Award for Neurohumoral Control’ in Acta Physiologica

2012 ◽  
Vol 206 (4) ◽  
pp. 209-212 ◽  
Author(s):  
L. Stjärne ◽  
P. B. Persson
Keyword(s):  
Author(s):  
Hans T. Versmold

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.


1983 ◽  
Vol 245 (4) ◽  
pp. G582-G588 ◽  
Author(s):  
W. J. Snape ◽  
S. Shiff

Colonic motility was examined in the proximal (taeniated) and distal (nontaeniated) colon of New Zealand White rabbits. Colonic myoelectric and contractile activities were recorded by bipolar electrodes and extraluminal strain gauges sewn on the antimesenteric serosal surface of the proximal and distal colon. Slow-wave frequency consistently was slower in the proximal colon (13.2 +/- 0.9) compared with the distal colon (15.8 +/- 1.2) (P less than 0.05). During the control period 81.8 +/- 5.2% of slow waves have superimposed spike potentials in the proximal colon. The distal colon had similar amounts of spike activity. The distal colon had increased base-line contractility (P less than 0.02). Atropine inhibited spike and contractile activity on both sides of the colon, but the distal colon still had more contractile activity than the proximal colon (P less than 0.02). The alpha-adrenergic agonist phenylephrine and antagonist phentolamine had no effect on colonic motility. Isoproterenol inhibited colonic smooth muscle spike and contractile activity. This effect was blocked by propranolol. Administration of trimethaphan camsylate caused an increase in spike and contractile activity only in the distal colon. The effect of trimethaphan on the distal colon was inhibited by atropine. These studies show that 1) tonic cholinergic stimulation exists both in the proximal and in the distal colon, 2) circulating catecholamines have minimal effect on base-line colonic motility, and 3) tonic nonadrenergic inhibition of the distal colon modulates the tonic cholinergic stimulation.


CHEST Journal ◽  
1982 ◽  
Vol 81 (5) ◽  
pp. 11-13 ◽  
Author(s):  
M.R. Knowles ◽  
G.F. Murray ◽  
J.A. Shallal ◽  
J.T. Gatzy ◽  
R.C. Boucher

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1025 ◽  
Author(s):  
Manfred J. Müller ◽  
Corinna Geisler ◽  
Steven B. Heymsfield ◽  
Anja Bosy-Westphal

Presently, control of body weight is assumed to exist, but there is no consensus framework of body weight homeostasis. Three different models have been proposed, with a “set point” suggesting (i) a more or less tight and (ii) symmetric or asymmetric biological control of body weight resulting from feedback loops from peripheral organs and tissues (e.g. leptin secreted from adipose tissue) to a central control system within the hypothalamus. Alternatively, a “settling point” rather than a set point reflects metabolic adaptations to energy imbalance without any need for feedback control. Finally, the “dual intervention point” model combines both paradigms with two set points and a settling point between them. In humans, observational studies on large populations do not provide consistent evidence for a biological control of body weight, which, if it exists, may be overridden by the influences of the obesogenic environment and culture on personal behavior and experiences. To re-address the issue of body weight homeostasis, there is a need for targeted protocols based on sound concepts, e.g. lean rather than overweight subjects should be investigated before, during, and after weight loss and weight regain. In addition, improved methods and a multi-level–multi-systemic approach are needed to address the associations (i) between masses of individual body components and (ii) between masses and metabolic functions in the contexts of neurohumoral control and systemic effects. In the future, simplifications and the use of crude and non-biological phenotypes (i.e. body mass index and waist circumference) should be avoided. Since changes in body weight follow the mismatch between tightly controlled energy expenditure at loosely controlled energy intake, control (or even a set point) is more likely to be about energy expenditure rather than about body weight itself.


Endocrinology ◽  
1953 ◽  
Vol 52 (2) ◽  
pp. 149-156 ◽  
Author(s):  
T. M. HUSTON ◽  
A. V. NALBANDOV
Keyword(s):  

1999 ◽  
Vol 15 (5) ◽  
pp. 380 ◽  
Author(s):  
Michael A. Shetzline ◽  
Rodger A. Liddle

2008 ◽  
Vol 295 (6) ◽  
pp. R1926-R1933 ◽  
Author(s):  
Jean C. Hardwick ◽  
E. Marie Southerland ◽  
Jeffrey L. Ardell

Chronic myocardial infarction (CMI) is associated with remodeling of the ventricle and evokes adaption in the cardiac neurohumoral control systems. To evaluate the remodeling of the intrinsic cardiac nervous system following myocardial infarction, the dorsal descending coronary artery was ligated in the guinea pig heart and the animals were allowed to recover for 7–9 wk. Thereafter, atrial neurons of the intrinsic cardiac plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic cardiac neurons demonstrated no significant changes in passive membrane properties or action potential configuration compared with age-matched controls and sham-operated animals. The intrinsic cardiac neurons from chronic infarcted hearts did demonstrate an increase in evoked action potential (AP) frequency (as determined by the number of APs produced with depolarizing stimuli) and an increase in responses to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide (PACAP)-induced increases in intrinsic cardiac neuron-evoked AP frequency were similar between control and CMI animals. Immunohistochemical analysis demonstrated a threefold increase in percentage of neurons immunoreactive for neuronal nitric oxide synthase (NOS) in CMI animals compared with control and the additional expression of inducible NOS by some neurons, which was not evident in control animals. Finally, the density of mast cells within the intrinsic cardiac plexus was increased threefold in preparations from CMI animals. These results indicate that CMI induces a differential remodeling of intrinsic cardiac neurons and functional upregulation of neuronal responsiveness to specific neuromodulators.


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