scholarly journals Increased Activity of the Autonomic Nervous System and Increased Sensitivity to Angiotensin II Infusion after Therapy with Recombinant Human Erythropoietin

Nephron ◽  
1990 ◽  
Vol 56 (2) ◽  
pp. 220-221 ◽  
Author(s):  
K. Jandeleit ◽  
B. Heintz ◽  
E. Gross-Heitfeld ◽  
J. Kindler ◽  
H.G. Sieberth ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Recombinant Human Erythropoietin ◽  
Autonomic Nervous ◽  
Human Erythropoietin ◽  
Increased Sensitivity ◽  
Increased Activity

scholarly journals Recombinant Human Erythropoietin Therapy and Autonomic Nervous System

Nephron ◽  
1992 ◽  
Vol 61 (1) ◽  
pp. 115-116 ◽  
Author(s):  
Junji Suwata ◽  
Hiroo Maeda ◽  
Nobuhiro Ohmori ◽  
Mahumi Ohwa ◽  
Hiroyuki Ohtsuka ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Recombinant Human Erythropoietin ◽  
Autonomic Nervous ◽  
Human Erythropoietin

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Similar Pattern ◽  
Ang Ii ◽  
Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

scholarly journals HORMONAL AND VEGETATIVE FACTORS OF INSULIN RESISTANCE IN PATIENTS WITH HYPERTENSION

2021 ◽  
Vol 77 (3) ◽  
pp. 91-98
Author(s):  
Sergii Shevchuk ◽  
Володимир Корчинський
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Parathyroid Hormone ◽  
Angiotensin Ii ◽  
Arterial Hypertension ◽  
Plasma Renin ◽  
Activity Levels ◽  
Central Hemodynamics ◽  
Autonomic Nervous

The combination of arterial hypertension (AH) and insulin resistance (IR) significantly increases the risk of cardiovascular complications. Research objective: Studying indices of carbohydrate metabolism, activity of renin-angiotensin-aldosterone system, calcium-regulating hormones, adrenal glucocorticoid function, the condition of the autonomic nervous system and their possible interrelation with hemodynamic parameters in AH patients with different insulin sensitivity. A comprehensive study of hormonal profile was held with use of radio immune method and that of central hemodynamics with use of echocardiography in 72 patients with arterial hypertension stage II, 1-2 degrees, male (mean age – 54.1±3.4 years), with a body mass index up to 30 kg / mІ and verified insulin resistance (IR), in 32 patients of which insulin resistance (IR) was revealed, and in 40 patients its absence was fixed. Insulin resistance was verified by the value of HOMA-IR in excess of 2,77. To assess the condition of the autonomic nervous system, studies of heart rate variability were performed. It is established that patients with hypertension with IR had increased level of plasma renin activity, levels of angiotensin II, cortisol, insulin, parathyroid hormone, decreased parasympathetic and increased sympathetic tonus. According to the results of factor analysis, AH with insulin resistance has a distinctive structure of neurohumoral regulation of the main indicators of central hemodynamics and interhormonal interactions; the direct regulatory effects of angiotensin II, insulin, progesterone, parathyroid hormone on the indicators of central hemodynamics, modulation of presorption action increases. The study not only revealed peculiarities of neurohumoral profiles in patients with hypertension depending on insulin resistance, but also determined distinctive features in structure of the regulatory process of central hemodynamics and interhormonal interactions. This should be taken into account when prescribing antihypertensive therapy.

Sympathetic Hyperfunction Causes Increased Sensitivity of the Autonomic Nervous System to Whole-Body X Irradiation

2005 ◽  
Vol 163 (2) ◽  
pp. 137-143 ◽  
Author(s):  
Mutsumi Matsuu ◽  
Kazuko Shichijo ◽  
Yuji Ikeda ◽  
Masahiro Ito ◽  
Shinji Naito ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Whole Body ◽  
Autonomic Nervous ◽  
X Irradiation ◽  
Increased Sensitivity

scholarly journals Role of AT1 receptors and autonomic nervous system in mediating acute pressor responses to ANG II in anesthetized mice

1999 ◽  
Vol 277 (5) ◽  
pp. E838-E847 ◽  
Author(s):  
Trinity J. Bivalacqua ◽  
Ajay Dalal ◽  
Hunter C. Champion ◽  
Philip J. Kadowitz
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Peripheral Resistance ◽  
Inhibitory Effects ◽  
Hemodynamic Responses ◽  
Autonomic Nervous ◽  
Pressor Responses ◽  
Cd1 Mice

Hemodynamic responses to angiotensin II and the role of AT1 and AT2 receptors and the autonomic nervous system in mediating acute responses to angiotensin II were investigated in anesthetized CD1 mice. Injections of angiotensin II caused dose-related increases in systemic arterial pressure that were antagonized by candesartan. Pressor responses to angiotensin II were not altered by PD-123,319 in doses up to 25 mg/kg iv. At the lowest dose studied (20 μg/kg iv), the inhibitory effects of candesartan were competitive, whereas at the highest dose (100 μg/kg iv) the dose-response curve for angiotensin II was shifted to the right in a nonparallel manner with inhibitory effects that could not be surmounted. The inhibitory effects of candesartan were selective and were similar in animals pretreated with enalaprilat (1 mg/kg iv) to reduce endogenous angiotensin II production. Acute pressor responses to angiotensin II were not altered by propranolol (200 μg/kg iv), phentolamine (200 μg/kg iv), or atropine (1 mg/kg iv) but were enhanced by hexamethonium (5 mg/kg iv). Increases in total peripheral resistance induced by angiotensin II were inhibited by the AT1-receptor antagonist but were not altered by AT2-, α-, or β-receptor antagonists. These results suggest that acute pressor responses to angiotensin II are mediated by AT1 receptors, are buffered by the baroreceptors, and are not modulated by effects on AT2 receptors and that activation of the sympathetic nervous system plays little if any role in mediating rapid hemodynamic responses to the peptide in anesthetized CD1 mice.

Systemic hemodynamic responses to chronic angiotensin II infusion into the renal artery of dogs

1997 ◽  
Vol 273 (6) ◽  
pp. R1980-R1989 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Kathleen M. Stevenson ◽  
Roger G. Evans ◽  
Warwick P. Anderson
Keyword(s):  
Nervous System ◽  
Cardiac Output ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Hemodynamics ◽  
Autonomic Ganglion ◽  
Autonomic Nervous

Chronic intrarenal infusion of angiotensin II (0.5 ng ⋅ kg−1⋅ min−1) in dogs increases arterial pressure. In the present study we determined whether this was associated with changes in cardiac output or in total peripheral resistance. Mean arterial pressure did not change initially but was significantly increased over days 14- 28 of the infusion period (+6 ± 2 mmHg), as was total peripheral resistance (+4 ± 2 mmHg ⋅ min ⋅ l−1). Neither cardiac output, renal blood flow, nor glomerular filtration rate was significantly changed over this period. To determine the influence of the autonomic nervous system on the developing hypertension, periodic acute autonomic ganglion blockade was performed. Before angiotensin II infusion ganglion blockade reduced total peripheral resistance and increased cardiac output, and this effect was similar across the 4 wk of angiotensin II infusion. Systemic hemodynamics were not affected by intravenous angiotensin II infusion (0.5 ng ⋅ kg−1⋅ min−1). Thus intrarenal infusion of low-dose angiotensin II produced a chronic increase in arterial pressure due to an action within the kidney. The hypertension was associated with increased total peripheral resistance but not with marked changes in cardiac output or renal function or in the influence of the autonomic nervous system on systemic hemodynamics.

Control of renal and mesenteric conductance during hemorrhage in conscious hypertensive rabbits

1996 ◽  
Vol 271 (4) ◽  
pp. H1531-H1540
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Autonomic Control ◽  
Ang Ii ◽  
Control Blood Pressure ◽  
Vascular Conductance ◽  
Autonomic Nervous ◽  
Impaired Ability

Control of renal and mesenteric conductance during hemorrhage was examined in conscious renal-wrap hypertensive rabbits. Hemorrhage was performed under control conditions and during blockade of 1) vasopressin (AVP) and angiotensin II (ANG II); 2) the autonomic nervous system (ANS); and 3) the ANS, AVP, and ANG II. We hypothesized that hypertensive rabbits would have impaired hormonal and autonomic control of renal and mesenteric conductance. When the ANS was intact, hypertensive rabbits had an impaired ability to control blood pressure but no impairment in renal and mesenteric vasoconstriction during hemorrhage. When the ANS was blocked, AVP- and ANG II-mediated control of blood pressure was not observed during hemorrhage but was observed during a 2-min pause after hemorrhage was terminated. During this pause (ANS blocked), the hypertensive rabbits did not exhibit an impaired vasoconstriction of the renal or mesenteric beds. We conclude that, although the hypertensive rabbits had an impaired ability to control blood pressure during hemorrhage, this was not associated with an impaired ANS- or AVP- and ANG II-mediated control of renal or mesenteric vascular conductance.

Pulmonary vascular responses to angiotensin II and captopril in conscious dogs

1986 ◽  
Vol 61 (4) ◽  
pp. 1552-1559 ◽  
Author(s):  
H. M. Goll ◽  
D. P. Nyhan ◽  
H. S. Geller ◽  
P. A. Murray
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pulmonary Circulation ◽  
Entire Range ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Autonomic Nervous

Our objectives were to investigate the extent to which angiotensin II (ANG II) and converting-enzyme inhibition (CEI) exert a direct vasoactive influence on the pulmonary circulation of conscious dogs. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by stepwise constriction of the thoracic inferior vena cava to reduce Q. The effects of ANG II infusion (60 ng X kg-1 X min-1, iv) and CEI with captopril (1 mg/kg plus 1 mg X kg-1 X h-1, iv) on pulmonary vascular P/Q plots were assessed first with the conscious dogs intact and again after combined administration of pharmacological antagonists to block sympathetic alpha- and beta-adrenergic, cholinergic, and arginine vasopressin receptors. In intact dogs, ANG II increased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure, PAP-PCWP) over the entire range of Q studied (60-120 ml X min-1 X kg-1). Conversely, CEI decreased (P less than 0.05) PAP-PCWP at each level of Q. After administration of the autonomic nervous system and arginine vasopressin receptor antagonists, ANG II again increased (P less than 0.01) and CEI decreased (P less than 0.01) PAP-PCWP over the entire range of Q studied. Thus exogenous administration of ANG II results in active, nonflow-dependent constriction of the pulmonary circulation, and this effect is not dependent on the autonomic nervous system or increased circulating levels of arginine vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

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