Plasma Noradrenaline Concentrations in Experimental Renovascular Hypertension in the Rat

1977 ◽  
Vol 52 (5) ◽  
pp. 477-483 ◽  
Author(s):  
H. J. Dargie ◽  
S. S. Franklin ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Experimental Hypertension ◽  
Hydroxylase Activity ◽  
Goldblatt Rat ◽  
Arterial Constriction ◽  
The One ◽  
6 Hydroxydopamine ◽  
Peripheral Sympathetic Activity

1. Plasma noradrenaline concentrations and dopamine β-hydroxylase activity have been measured at various stages in the development of hypertension in the one-kidney Goldblatt rat (unilateral renal arterial constriction and contralateral nephrectomy). 2. Although plasma noradrenaline concentrations were significantly elevated from control values at 7, 14 and 28 days, plasma dopamine β-hydroxylase activity was not significantly different from control values except at 24 h. 3. These findings suggest that peripheral sympathetic activity is increased in the one-kidney Goldblatt model of experimental hypertension but that plasma dopamine β-hydroxylase activity is a poor index of this increase. 4. Both the rise in blood pressure and the rise in plasma noradrenaline concentrations were prevented by pretreatment with intracisternal 6-hydroxydopamine, suggesting that the increased sympathetic activity is at least in part centrally mediated.

Nervous System and Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 45s-56s ◽  
Author(s):  
J. P. Chalmers
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Nervous System ◽  
Arterial Pressure ◽  
High Blood Pressure ◽  
Sympathetic Activity ◽  
Experimental Hypertension ◽  
Primary Role ◽  
Noradrenergic Nerves ◽  
Peripheral Sympathetic Activity

1. Presynaptic regulation. The regulation of noradrenaline release by a wide variety of substances acting on presynaptic receptors suggests that local factors may play a greater role in the control of blood pressure than was previously believed and that a number of new approaches to the drug treatment of hypertension could be developed. It also raises the possibility that there might be differences in the presynaptic receptor populations of hypertensive and normotensive subjects or animals. 2. Central nerve pathways. There is a need for more precise delineation of central nerve tracts subserving a cardiovascular function and for greater use of morphological techniques to confirm the reliability of biochemical and physiological experiments in the central nervous system. Two appropriate techniques are described. 3. Models of experimental hypertension. (a) Neurogenic hypertension: interference with baroreceptor afferents can cause a permanent elevation of arterial pressure mediated by increased activity of peripheral sympathetic nerves and of descending noradrenergic nerves terminating in the spinal cord. Catecholamine nerve connections of the nucleus tractus solitarius serve mainly to modulate rather than to mediate baroreceptor reflexes. (b) DOCA—salt hypertension: increased peripheral sympathetic activity is important in both the initiation and the maintenance of this form of hypertension. The decrease in brain-stem noradrenaline turnover found in this model could play a determinant role in the development of the high blood pressure. (c) Renal hypertension: both central and peripheral nervous mechanisms contribute to the development and the early phase of ‘one-kidney’ hypertension in animals. Their role in the maintenance of this form of hypertension is still controversial. (d) Spontaneously hypertensive rats: peripheral and central mechanisms do not appear to have a major role in the maintenance of this form of hypertension. However, it seems possible that centrally evoked increases in peripheral sympathetic activity could be important in the initiation of the high blood pressure. (e) Central catecholamines and blood pressure control; central catecholaminergic nerves do not make up a single homogeneous system. For example, the activity of descending noradrenergic nerves in the spinal cord contributes to an elevation of arterial pressure, whereas the activity of catecholaminergic nerves in the dorsomedial medulla appears to have a depressor effect. 4. Human essential hypertension. (a) There is no good evidence that the nervous system plays the major primary role in the development or maintenance of essential human hypertension. (b) Effective treatment of raised blood pressure through nervous mechanisms requires an understanding of the factors that normally control the pressure and does not necessarily depend on reversing specific nervous processes responsible for producing the increase in pressure.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1943 ◽  
Vol 77 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Harry Goldblatt ◽  
Joseph R. Kahn ◽  
Harvey A. Lewis
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renal Hypertension ◽  
Renal Arteries ◽  
Experimental Hypertension ◽  
Long Duration ◽  
Humoral Mechanism ◽  
Main Renal Artery ◽  
Experimental Renal Hypertension ◽  
The One

Persistent hypertension has been produced in the goat and sheep by constriction of the main renal arteries. The presence or absence of accompanying uremia depends upon the degree of constriction of the renal arteries. In both sheep and goat, constriction of one main renal artery also caused elevation of the blood pressure which tended to persist longer than in the dog. Excision of the one kidney with main renal artery constricted resulted in a prompt (24 hours) return of the blood pressure to normal. In the animals with hypertension of long duration but without renal excretory insufficiency, (the "benign" phase) no significant arterio- or arteriolosclerosis developed as a result of the hypertension alone. In the animals that had both hypertension and renal excretory insufficiency, (the "malignant" phase) the typical terminal arteriolar lesions developed in many organs. These lesions consisted of necrosis and fibrinoid degeneration of arterioles and necrotizing arteriolitis which should not be confused with arteriolosclerosis. The same humoral mechanism which is responsible for experimental renal hypertension in the dog and other animals also obtains in the pathogenesis of experimental renal hypertension in the sheep and goat.

Plasma Noradrenaline Concentration and α-Adrenoceptor-Mediated Vasoconstriction in Normotensive and Hypertensive Man

1981 ◽  
Vol 60 (5) ◽  
pp. 483-489 ◽  
Author(s):  
W. Kiowski ◽  
F. R. Bühler ◽  
P. Vanbrummelen ◽  
F. W. Amann
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Arterial Infusion ◽  
Hypertensive Patients ◽  
Noradrenaline Concentration ◽  
Normotensive Subjects ◽  
Control Plasma

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the α-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P<0.01) as well as the height of mean blood pressure (r = 0.73, P<0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the α-adrenoceptor-mediated component of vascular resistance.

Plasma Catecholamines do Not Invariably Reflect Sympathetically Induced Changes in Blood Pressure in Man

1983 ◽  
Vol 65 (3) ◽  
pp. 227-235 ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
Luisa Gregorini ◽  
G. Leonetti ◽  
G. Parati ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Plasma Noradrenaline ◽  
Carotid Baroreceptor ◽  
Induced Changes ◽  
Neck Chamber ◽  
Noradrenaline And Adrenaline

1. Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). 2. During the pressor response (15 ± 3 mmHg, mean ± se) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (−9 ± 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. 3. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with- a return to pretilting values no more than 4 min after resumption of the supine position. 4. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.

Sympathetic system in potassium homeostasis

1981 ◽  
Vol 241 (2) ◽  
pp. F151-F155 ◽  
Author(s):  
P. Silva ◽  
K. Spokes
Keyword(s):  
Serum Potassium ◽  
Sympathetic Activity ◽  
Volume Of Distribution ◽  
Sympathetic System ◽  
Insulin Deficiency ◽  
Chemical Sympathectomy ◽  
Renal Uptake ◽  
6 Hydroxydopamine ◽  
Peripheral Sympathetic Activity ◽  
Adrenalectomized Rats

The extrarenal disposal of potassium was studied in nephrectomized and adrenalectomized rats by measuring the rise in serum potassium produced during an infusion of 3 meq KCl/kg over 90 min. Adrenalectomy alone did not alter the volume of distribution of infused potassium in nephrectomized animals. When nephrectomy and adrenalectomy were combined with either insulin deficiency produced by streptozotocin or chemical sympathectomy induced by injection of 6-hydroxydopamine, potassium tolerance was significantly impaired. Hyperkalemia produced in chemically sympathectomized animals by potassium infusion was minimized by simultaneous infusion of epinephrine, an effect blocked by the beta-antagonist propranolol but not by the alpha-blocker phenoxybenzamine. These results suggest that extra renal uptake of potassium, in addition to being influenced by insulin and circulating catecholamines, is modulated by peripheral sympathetic activity.

Sequential Changes in Plasma Noradrenaline during Bicycle Exercise

1980 ◽  
Vol 58 (1) ◽  
pp. 37-43 ◽  
Author(s):  
R. D. S. Watson ◽  
C. A. Hamilton ◽  
D. H. Jones ◽  
J. L. Reid ◽  
T. J. Stallard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Supine Position ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Bicycle Exercise ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Exercise Blood Pressure ◽  
Venous Plasma

1. Forearm venous plasma noradrenaline, heart rate and intra-arterial blood pressure were measured sequentially during and after upright bicycle exercise in five normotensive and six hypertensive patients. 2. Plasma noradrenaline increased significantly between 4 and 8 min during exercise. 3. On stopping exercise blood pressure and heart rate decreased rapidly whilst plasma noradrenaline increased in each subject to reach a maximum at a median time of 108 s after exercise. 4. Plasma noradrenaline decreased in five of six normotensive patients between the end of exercise and 2 min after exercise performed in the supine position. 5. Evidence in favour of a reflex increase in sympathetic activity after upright exercise is discussed.

Erythrocyte Catechol-O-Methyltransferase Activity and Indices of Sympathetic Activity in Man

1980 ◽  
Vol 58 (5) ◽  
pp. 423-425 ◽  
Author(s):  
G. A. Fitzgerald ◽  
C. A. Hamilton ◽  
D. H. Jones ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Interindividual Variability ◽  
Population Sample ◽  
Plasma Noradrenaline ◽  
Methyltransferase Activity ◽  
Urinary Catecholamines ◽  
Wide Interindividual Variability ◽  
Inactivation Of Noradrenaline

1. Erythrocyte catechol-O-methyltransferase was studied in a population sample of 147 subjects. 2. There was a wide interindividual variability of catechol-O-methyltransferase activity, which was not unimodally distributed. Catechol-O-methyltransferase activity was not influenced by blood pressure, age or sex, nor was it related to plasma noradrenaline or urinary catecholamines or metanephrines. 3. It is not likely that inactivation of noradrenaline by O-methylation at least by erythrocytes is an important mechanism determining plasma noradrenaline, let alone arterial pressure.

Plasma noradrenaline in Goldblatt models of renovascular hypertension in the rat, before and after surgical reversal

1986 ◽  
Vol 71 (2) ◽  
pp. 199-204 ◽  
Author(s):  
S. M. Walker ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Early Phase ◽  
Sympathetic Activity ◽  
Chronic Phase ◽  
Plasma Noradrenaline ◽  
Before And After ◽  
Sympathetic Nervous ◽  
2K1c Hypertension

1. Plasma noradrenaline (NA), blood pressure (BP) and heart rate (HR) were measured simultaneously in conscious rats under basal conditions in the early phase (4–6 weeks) of one-kidney, one-clip hypertension (1K1C), in the early (4–6 weeks) and chronic (> 16 weeks) phases of the two-kidney, one-clip model (2K1C) and in age-matched loose clip control animals before and 2 days after unclipping. 2. The elevated BP in all three hypertensive groups fell to normal after unclipping, whereas removal of the constricting clip in loose clip controls had no effect on BP. 3. Plasma NA was elevated in 1K1C hypertension (P < 0.05) and fell slightly but non-significantly on unclipping. However, in the early phase of 2K1C hypertension plasma NA was unaltered before and rose significantly (P < 0.05) after unclipping. Plasma NA did not change with unclipping in the chronic phase of 2K1C hypertension and was not different from controls. Unclipping loose clip control animals produced no change in plasma NA. 4. Changes in HR on unclipping followed a similar pattern to changes in plasma NA: changes in the two variables were significantly correlated in all three models (1K1C: r = 0.61, P < 0.005; early 2K1C: r = 0.45, P < 0.05; chronic 2K1C: r = 0.62, P < 0.01). However, BP was only correlated with plasma NA in 1K1C hypertension (r = 0.49, P < 0.02) and not in either phase of the 2K1C model. There was also a highly significant correlation between HR and plasma NA in 1K1C hypertension (r = 0.71, P < 0.001). The pattern of the changes in plasma NA and HR that occurred with reversal of 1K1C hypertension was significantly different from those in the early phase 2K1C model (P < 0.05). 5. These data suggest that there is sympathetic nervous system (SNS) activation in the early phase of 1K1C hypertension, but provide no evidence for increased sympathetic activity in either the early or chronic phases of the 2K1C model. Neither do they support the hypothesis that the fall in BP with unclipping in this model is mediated by reduced SNS activity.

Clonidine and Sympathetic Activity during Sleep

1979 ◽  
Vol 57 (6) ◽  
pp. 509-514 ◽  
Author(s):  
T. J. B. Maling ◽  
C. T. Dollery ◽  
C. A. Hamilton
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Slow Release ◽  
Paradoxical Sleep ◽  
Plasma Noradrenaline ◽  
Sleep Period ◽  
Blood Pressure Fall ◽  
Before And After ◽  
Pressure Fall ◽  
Healthy Males

1. Blood pressure, heart rate, plasma noradrenaline and electroencephalographic variables were measured simultaneously during sleep in five healthy males before and after slow-release clonidine (300 μg orally) or placebo. 2. The blood pressure fall during sleep correlated significantly with the depth of sleep. 3. Clonidine significantly reduced systolic blood pressure during sleep and profoundly reduced total paradoxical sleep duration. 4. Plasma noradrenaline declined progressively during the sleep period and concentrations were significantly lower after clonidine compared with placebo.

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