Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man

1987 ◽  
Vol 112 (1) ◽  
pp. 145-150 ◽  
Author(s):  
S. Al-Damluji ◽  
D. Cunnah ◽  
A. Grossman ◽  
L. Perry ◽  
G. Ross ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Biological Effects ◽  
Random Order ◽  
Normal Male ◽  
Plasma Acth ◽  
Plasma Adrenaline ◽  
Corticotrophin Releasing Factor ◽  
Cortisol Responses ◽  
Male Subjects ◽  
Single Blind

ABSTRACT Six normal male subjects were given, in single blind random order on six separate occasions, i.v. bolus doses of synthetic ovine corticotrophin-releasing factor-41 (oCRF-41; 25 and 50 μg) with and without adrenaline (3 μg/min) i.v. for 150 min, the adrenaline infusions alone and saline placebo. The adrenaline infusions resulted in plasma adrenaline concentrations of 4·33 ± 0·82 (s.e.m.) nmol/l and were associated with an increase in blood glucose, heart rate and systolic blood pressure and a reduction of diastolic blood pressure. Despite these evident biological effects at several sites, there was no stimulation of plasma ACTH or cortisol by adrenaline in comparison with the effect of saline, and no enhancement of the stimulatory effect of either dose of oCRF-41 on ACTH or cortisol secretion. The ACTH response to 50 μg oCRF-41 was greater than that to 25 μg, indicating that the 25 μg dose of oCRF-41 was sub-maximal and capable of further enhancement. As the plasma adrenaline concentrations during the adrenaline infusions reached the upper limit of the physiological range of plasma adrenaline in man, yet failed to enhance the ACTH or cortisol responses to a sub-maximal dose of oCRF-41, we conclude that circulating adrenaline neither exerts a direct stimulatory effect on pituitary corticotrophs nor enhances the effect of CRF under physiological circumstances. The adrenaline infusions attenuated the ACTH and cortisol responses to oCRF-41 and were associated with a transient reduction of basal concentrations of both hormones. J. Endocr. (1987) 112, 145–150

Increase in Prostaglandins during Converting Enzyme Inhibition

1980 ◽  
Vol 59 (s6) ◽  
pp. 133s-135s ◽  
Author(s):  
S. L. Swartz ◽  
G. H. Williams ◽  
N. K. Hollenberg ◽  
F. R. Crantz ◽  
L. Levine ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Concentration ◽  
Sodium Intake ◽  
Thromboxane A2 ◽  
Normal Male ◽  
Converting Enzyme ◽  
Low Sodium ◽  
Converting Enzyme Inhibition ◽  
Male Subjects ◽  
Hypotensive Response

1. Because changes in the plasma concentration of angiotensin II and bradykinin appear inadequate to account completely for the hypotensive response to captopril, we measured changes in plasma prostaglandins in response to increasing doses of captopril in nine supine normal male subjects studied on both a high (200 mol/l) and low (10 mol/l) sodium intake. 2. On both the high and low sodium diets, captopril induced significant (P<0.01) increments in the 13,14-dihydro-15-keto metabolite of the vasodilatory prostaglandin E2, which correlated significantly with the fall in blood pressure (P<0.0001). 3. No significant changes were noted in the plasma levels of 6-keto-prostaglandins F1α or thromboxane B2, the stable products of prostacyclin and thromboxane A2 respectively.

Effect of Single and Combined Infusions of Angiotensin II and Aldosterone on Colonic Potential Difference, Blood Pressure and Renal Function, in Patients with Adrenal Deficiency

1975 ◽  
Vol 48 (3) ◽  
pp. 219-226
Author(s):  
A. D. Efstratopoulos ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Concentrations ◽  
Young Male ◽  
Normal Subjects ◽  
Potential Difference ◽  
Normal Male ◽  
Adrenal Deficiency ◽  
Increased Sensitivity ◽  
Male Subjects

1. The effect of single and combined infusions of angiotensin and aldosterone on colonic potential difference, blood pressure and renal function was studied in two normal male subjects and four female patients with adrenal deficiency maintained only on cortisone. 2. Aldosterone had its usual effect on colonic potential difference and it was possible to show that angiotensin had a small but definite effect of its own in the absence of aldosterone. The two hormones produced a summation response when given together. 3. The effects on renal function in two normal young male subjects were similar to those known previously. The response of the patients was different and probably reflected a number of factors, such as age, sex and long-standing adrenal deficiency. 4. Although the numbers were small, both normal subjects and patients showed a significantly greater rise of blood pressure with combined infusions of angiotensin and aldosterone than with angiotensin alone. The plasma concentrations of angiotensin were similar with both types of infusion, and so increased sensitivity to angiotensin in the presence of aldosterone is postulated.

Effect of Acute Mild Hypoglycaemia on Counterregulatory Responses to Moderate Hypoglycaemia Induced Immediately Afterwards in Healthy Men

1993 ◽  
Vol 85 (5) ◽  
pp. 537-542 ◽  
Author(s):  
K. T. Moriarty ◽  
E. J. Simpson ◽  
N. S. Brown ◽  
I. A. MaCdonald ◽  
R. B. Tattersall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Glucose ◽  
Symptom Score ◽  
Random Order ◽  
Sweating Rate ◽  
Hormonal Responses ◽  
Healthy Men ◽  
Mild Hypoglycaemia ◽  
Single Blind

1. This study was designed to determine whether a 1 h period of mild hypoglycaemia (33 or 3.7 mmol/l) affected the response to an episode of moderate hypoglycaemia (2.5 mmol/l) immediately afterwards. 2. Eleven non-obese healthy men (age 26 + 1 years, mean + SEM) underwent three separate 3 h hyperinsulinaemic glucose clamps in single-blind, random order. On all three occasions, blood glucose was 4.5 mmol/l for the first hour, and on a control visit was maintained at this level for the second hour. In the other two visits, blood glucose was lowered to 3.7 or 33 mmol/l during the second hour. In the third hour, blood glucose was lowered to 2.5 mmol/l on all three visits. 3. In the second hour, adrenaline rose significantly (P <0.05, analysis of variance) with a blood glucose of 33 and 3.7 mmol/l, as did cortisol and heart rate at 33 mmol/l, but glucagon, prolactin, sweating rate, symptom score and blood pressure were the same during the second hour on all three visits. 4. In the final hour at 2.5 mmol/l, there were no differences in adrenaline, noradrenaline, glucagon, prolactin, cortisol, symptom score, heart rate, blood pressure or sweating rate. 5. Thus, the overall magnitude of hormonal responses to moderate hypoglycaemia (2.5 mmol/l) are not modified by exposure to mild hypoglycaemia (33 or 3.7 mmol/l) for 1 h immediately beforehand.

Differential effect of high-dose naloxone on the plasma adrenaline response to the cold-pressor test

1989 ◽  
Vol 76 (6) ◽  
pp. 625-630 ◽  
Author(s):  
P. M. G. Bouloux ◽  
E. Newbould ◽  
R. Causon ◽  
L. Perry ◽  
L. H. Rees ◽  
...  
Keyword(s):  
Randomized Study ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Significant Rise ◽  
Plasma Noradrenaline ◽  
Normal Male ◽  
High Dose ◽  
Plasma Acth ◽  
Plasma Adrenaline ◽  
Pressor Test

1. Although the opiate antagonist naloxone has been shown to affect sympathoadrenomedullary function in some studies, this has not been a uniform finding in all investigations, using different doses of naloxone. We have therefore investigated the actions of saline placebo and increasing bolus doses of intravenous naloxone (25, 100 and 250 μg/kg) on the plasma noradrenaline, adrenaline, adrenocorticotrophin (ACTH) and cortisol responses to a cold-pressor test in six males and two females in a double-blind randomized study. 2. Basal levels of adrenaline did not differ on any of the study occasions: the cold-pressor stimulus produced a significant rise in mean plasma adrenaline to a peak of 0.16 nmol/l, with a peak incremental rise of 0.08 nmol/l. In the presence of the two higher doses of naloxone, the incremental rise in the mean adrenaline level was significantly enhanced, reaching 0.30 nmol/l at 100 μg of naloxone/kg and 0.29 nmol/l at 250 μg of naloxone/kg, with no significant enhancement observed at the lowest dose of naloxone. The rise in plasma noradrenaline, systolic and diastolic blood pressure and pulse rate during the cold-pressor test was not consistently altered by any dose of naloxone, but there was a significant trend for the degree of discomfort to increase with the dose of naloxone. 3. Neither plasma ACTH nor serum cortisol rose in response to the cold-pressor stimulus. Analysis of variance demonstrated a significant naloxone-treatment effect for both ACTH and cortisol, with the 100 μg/kg and 250 μg/kg doses of naloxone leading to a significant rise in mean plasma ACTH not seen at the lowest dose of 25 μg/kg. 4. In a separate study of the effect of naloxone on the clearance of plasma adrenaline, adrenaline was infused on two occasions into eight normal male subjects to a maximum dose of 5 μg/min for 15 min, and blood was sampled at regular intervals during and after termination of the infusion, preceded by 8 mg of naloxone or placebo. After termination of the adrenaline infusion, there was a rapid fall in plasma adrenaline (Λ = −1.9 ± 0.3 min), which was not altered by naloxone (Λ = −1.8 ± 0.3 min). 5. We conclude that the potentiation of the adrenaline response to a cold-pressor test by naloxone is mediated by increased secretion of adrenaline and not by a reduction in its clearance rate, and that this response is of low naloxone sensitivity.

Effects of Angiotensin II and Aldosterone on Diastolic Function In Vivo in Normal Man

1994 ◽  
Vol 87 (4) ◽  
pp. 397-401 ◽  
Author(s):  
P. B. M. Clarkson ◽  
N. M. Wheeldon ◽  
C. MacLeod ◽  
M. Tennent ◽  
T. M. MacDonald
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Diastolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Normal Male ◽  
Normal Man ◽  
Male Subjects ◽  
Left Ventricular Diastolic Filling

1. Doppler echocardiographic indices of diastolic function and systemic haemodynamics were studied in response to infusions of angiotensin II (1, 2, 5 and 10 ng min−1 kg−1), D-aldosterone (2, 4, 10 and 20 ng min−1 kg−1) and placebo [0.9% (w/v) NaCl] in ten normal male subjects. 2. Dose-related increases in systolic and diastolic blood pressure were observed with angiotensin II infusion at rates of 2 ng min−1 kg−1 and above, whereas no changes in blood pressure occurred with D-aldosterone. No changes in aortic stroke distance or heart rate were seen with either angiotensin II or aldosterone infusion. 3. Compared with placebo, angiotensin II infusion produced a dose-related prolongation of the isovolumic relaxation time [mean and 95% confidence intervals 12.0 (8.2–15.8) ms, P < 0.001] at 10 ng min−1 kg−1, and a significant reduction in the ratio between early and late transmitral flow velocity integrals at 2 ng min−1 kg−1, [−0.84 (−1.63 to −0.05), P < 0.05] and 5 ng min−1 kg−1 [−0.76 (−1.47 to −0.05), P < 0.05]. No changes in Doppler echocardiographic indices of diastolic function were observed with D-aldosterone infusion. 4. These data suggest that angiotension II, even at a sub-pressor concentration, produces an impairment of left ventricular diastolic filling, which occurs independently of its effect on aldosterone release.

The physiological significance of arginine vasopressin in potentiating the response to corticotrophin-releasing factor in sheep

1986 ◽  
Vol 108 (2) ◽  
pp. 309-312 ◽  
Author(s):  
C. Redekopp ◽  
J. H. Livesey ◽  
W. Sadler ◽  
R. A. Donald
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Physiological Significance ◽  
Plasma Acth ◽  
Physiological Importance ◽  
Corticotrophin Releasing Factor ◽  
Acth Concentration ◽  
Cortisol Responses ◽  
Hypertonic Saline Infusion

ABSTRACT In order to assess the physiological importance of endogenous arginine vasopressin (AVP) in augmenting the ACTH response to corticotrophin-releasing factor (CRF), the response to CRF during hypertonic saline infusion in six Coopworth sheep was examined. A 4-h infusion of 5% (w/v) NaCl (3·8 ml/min) resulted in significantly (P < 0·01) greater rises in ACTH and cortisol, but not aldosterone, than were observed after CRF alone. Infusion of hypertonic saline without CRF resulted in a highly significant (P < 0·001) rise in plasma osmolality and AVP but no significant change in plasma ACTH, cortisol or aldosterone. It is concluded that a marked but physiological increase in peripheral (and presumably central) levels of AVP does not result in any demonstrable change in plasma ACTH concentration. However, under these conditions, the ACTH and cortisol responses to CRF are considerably augmented. J. Endocr. (1986) 108, 309–312

Responses of ACTH, epinephrine, norepinephrine, and cardiovascular system to hemorrhage

1986 ◽  
Vol 251 (3) ◽  
pp. H612-H618 ◽  
Author(s):  
D. N. Darlington ◽  
J. Shinsako ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Random Order ◽  
Plasma Acth ◽  
Arterial Blood ◽  
The Relationship ◽  
Subsequent Rise

Hemorrhages of various magnitudes were performed on conscious rats, and arterial pressure, heart rate, and plasma levels of adrenocorticotropin hormone (ACTH), epinephrine, and norepinephrine were measured. Eight rats were prepared with chronic femoral arterial cannulas and received a 10, 15, or 20 ml/kg X 3 min hemorrhage in random order on day 4, 7, or 10 after surgery. Mean arterial blood pressure, heart rate, and plasma ACTH, epinephrine, and norepinephrine concentrations were determined before and 20 min after hemorrhage. Arterial blood pressure decreased significantly immediately after each hemorrhage and slowly recovered over the next 20 min. Heart rate did not change during the 10 ml/kg X 3 min hemorrhage but decreased significantly after 15 and 20 ml/kg X 3 min hemorrhages. Plasma ACTH and epinephrine levels increased significantly 20 min after the 15 and 20 ml/kg X 3 min hemorrhages but not after 10 ml/kg X 3 min hemorrhage. Norepinephrine increased significantly 20 min after the 20 ml/kg X 3 min hemorrhage but not after the 10 or 15 ml/kg X 3 min hemorrhage. There was no significant effect of time and repeated hemorrhages on resting levels of plasma ACTH, epinephrine, norepinephrine, osmolality, or proteins. Since hemorrhage leads to a fall in arterial pressure and a subsequent rise in plasma ACTH, the relationship between plasma ACTH and mean arterial blood pressure during hemorrhage was examined in both conscious and acutely prepared pentobarbital sodium-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The Influence of Acute Starvation on the Cardiovascular Responses to Lower Body Subatmospheric Pressure or to Standing in Man

1984 ◽  
Vol 66 (2) ◽  
pp. 141-146 ◽  
Author(s):  
T. Bennett ◽  
I. A. MacDonald ◽  
R. Sainsbury
Keyword(s):  
Blood Pressure ◽  
Nervous Activity ◽  
Cardiovascular Responses ◽  
Sympathetic Nervous Activity ◽  
Normal Male ◽  
Lower Body ◽  
Subatmospheric Pressure ◽  
Acute Starvation ◽  
Male Subjects ◽  
Forearm Vascular Resistance

1. The cardiovascular responses to lower body subatmospheric pressure or to standing were measured in the same nine normal male subjects after a 12 h and after a 48 h fast. 2. After the 48 h fast there was a significant reduction in diastolic blood pressure and forearm vascular resistance (relative to the values after a 12 h fast) when subjects were supine. 3. During exposure to lower body subatmospheric pressure, subjects who had fasted for 48 h showed an inability to maintain systolic blood pressure, accompanied by an impairment of forearm vasoconstriction and an exaggerated tachycardia (relative to their responses after a 12 h fast). Similar disorders of cardiovascular homoeostasis were seen on standing. 4. The results are consistent with an inhibition of sympathetic nervous activity after a 48 h fast, but other possibilities are discussed.

The Physiological Effects of Insulin-Induced Hypoglycaemia in Man: Responses at Differing Levels of Blood Glucose

1983 ◽  
Vol 65 (3) ◽  
pp. 263-271 ◽  
Author(s):  
E. A. M. Gale ◽  
T. Bennett ◽  
I. A. MacDonald ◽  
J. J. Holst ◽  
J. A. Matthews
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Plasma Glucose ◽  
Bolus Injection ◽  
Severe Hypoglycaemia ◽  
Normal Male ◽  
Neural Responses ◽  
Cortisol Responses ◽  
Rate Of Recovery ◽  
Hormone Responses

1. The aim of this study was to describe hormonal, cardiovascular and thermoregulatory responses to insulin-induced hypoglycaemia of differing levels of severity. 2. Five normal male volunteers were rendered hypoglycaemic at intervals of 1 week by intravenous infusions of 3, 4 or 6 units of insulin/h, or by intravenous injection of 0.15 unit/kg body weight. 3. Plasma glucose reached nadir values of 2.08 ±0.10, 1.82 ± 0.21, 1.24 ±0.08 and 0.92 ± 0.06 mmol/l (means ± sem) in the four experiments. Non-esterified fatty acid levels fell equally in all experiments but recovery was more rapid with severe hypoglycaemia. In contrast the rate of recovery of plasma glucose was slower with deeper hypoglycaemia and this appeared unrelated to the counter-regulatory response. 4. Plasma glucagon, adrenaline and prolactin levels increased in proportion to the severity of hypoglycaemia, but peak concentrations of cortisol, growth hormone (somatotropin) and noradrenaline did not vary, suggesting that moderate hypoglycaemia had elicited maximal responses. When the areas under the curves were calculated, the cortisol responses were greater for the 6 units infusion and bolus injection than for the other infusions, and the growth hormone responses were similar for all three infusions but significantly greater with the bolus injection. 5. Increases in heart rate and systolic blood pressure were related to the severity of hypoglycaemia, but changes in diastolic blood pressure and peripheral vascular resistance (assessed from calf and from hand blood flow) were not. 6. Central temperature fell by 0.13 ± 0.06°C, 0.30 ± 0.10°C, 0.65 ± 0.14°C and 1.15 ± 0.30°C (means ± sem) in the four experiments, and the fall in skin temperature had a similar gradation. 7. Many physiological responses to hypoglycaemia are not ‘all-or-none’, but vary according to the intensity of stimulus; some are already maximal at mild degrees of hypoglycaemia. Other changes are more complex, reflecting an interplay between opposing endocrine and neural responses.

Effects of variations in intragastric volume on blood pressure and splanchnic blood flow during intraduodenal glucose infusion in healthy older subjects

2012 ◽  
Vol 302 (4) ◽  
pp. R391-R399 ◽  
Author(s):  
Lora Vanis ◽  
Diana Gentilcore ◽  
Kylie Lange ◽  
Odd Helge Gilja ◽  
Rachael S. Rigda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Random Order ◽  
Glucose Infusion ◽  
Splanchnic Blood Flow ◽  
Gastric Distension ◽  
Plasma Norepinephrine ◽  
Older Subjects ◽  
Male Subjects ◽  
Mesenteric Vascular Resistance

The postprandial reduction in blood pressure (BP) is triggered by the interaction of nutrients with the small intestine and associated with an increase in splanchnic blood flow. Gastric distension may attenuate the postprandial fall in BP. The aim of this study was to determine the effects of differences in intragastric volume, including distension at a low (100 ml) volume, on BP and superior mesenteric artery (SMA) blood flow responses to intraduodenal glucose in healthy older subjects. BP and heart rate (HR; automated device), SMA blood flow (Doppler ultrasound), mesenteric vascular resistance (MVR), and plasma norepinephrine of nine male subjects (65–75 yr old) were measured after an overnight fast on 4 separate days in random order. On each day, subjects were intubated with a nasoduodenal catheter, incorporating a duodenal infusion port, and orally with a second catheter, incorporating a barostat bag, positioned in the fundus. Each subject received a 60-min ( t = 0–60 min) intraduodenal glucose infusion (3 kcal/min) and gastric distension at a volume of 1) 0 ml (V0), 2) 100 ml (V100), 3) 300 ml (V300), or 4) 500 ml (V500). Systolic BP fell ( P < 0.05) during V0, but not during V100, V300, or V500. In contrast, HR ( P < 0.01) and SMA blood flow ( P < 0.001) increased and MVR decreased ( P < 0.05) comparably on all 4 days. Plasma norepinephrine rose ( P < 0.01) in response to intraduodenal glucose, with no difference between the four treatments. There was a relationship between the areas under the curve for the change in systolic BP from baseline with intragastric volume ( r = 0.60, P < 0.001). In conclusion, low-volume (≤100 ml) gastric distension has the capacity to abolish the fall in BP induced by intraduodenal glucose in healthy older subjects without affecting SMA blood flow or MVR. These observations support the concept that nonnutrient gastric distension prior to a meal has potential therapeutic applications in the management of postprandial hypotension.

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