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

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.

1965 ◽  
Vol 209 (4) ◽  
pp. 844-848 ◽  
Author(s):  
John R. Gill ◽  
Kenneth L. Melmon ◽  
Louis Gillespie ◽  
Frederic C. Bartter

Renal function was studied in five normal subjects during the infusion of bradykinin at 0.1 and 0.4 µg/kg per min, and in four additional normal subjects during the infusion of norepinephrine at dosages beginning with 1–3 µg/ min. Bradykinin at both dosages decreased glomerular filtration rate (GFR) and tended to increase renal blood flow (ERPF). It increased sodium excretion (UNaV) at the lower dosage, but did not increase it further at the higher dosage. At all dosages, norepinephrine decreased ERPF and UNaV. The effects of bradykinin cannot be explained solely as effects of norepinephrine released by the bradykinin. During adrenergic blockade produced by guanethidine, bradykinin, 0.1 µg/kg per min, slightly decreased GFR and UNaV; at 0.4 µg/kg per min, it further decreased GFR and UNaV and tended to decrease ERPF as well. It did not lower blood pressure. The data suggest that in normal man, bradykinin increases UNaV only at low dosages. During adrenergic blockade, endogenous release of angiotensin could have prevented bradykinin from lowering blood pressure and could have caused the decreases in GFR, ERPF, and UNaV. A possible role is suggested for bradykinin in the physiologic control of renal function, and as a causative agent in producing the changes in renal function found in certain disease states characterized by excessive production of kinins.


1983 ◽  
Vol 3 (4) ◽  
pp. 442-447 ◽  
Author(s):  
Lawrence C. McHenry ◽  
David A. Stump ◽  
George Howard ◽  
Thomas T. Novack ◽  
Don H. Bivins ◽  
...  

A single-blind study was conducted in 13 right-handed normal male subjects to compare the effects of oral and i.v. papaverine on regional cerebral blood flow (rCBF). Six xenon-133 inhalation rCBF measurements were performed on each subject; three tests—baseline, placebo, and drug evaluations—were carried out on each of two separate days. The oral and i.v. drugs were randomized for first-day administration. rCBF, measured as flow gray (FG), increased significantly (p ≤ 0.001) from baseline with both drug forms. Increases of 10.53% and 13.94% (left and right hemispheres, respectively) were demonstrated 90 min after a single 600-mg dose of oral papaverine. Increases of 5.09% and 8.69%, respectively, were recorded immediately after a single 100-mg dose of i. v. papaverine. FG also increased significantly (p ≤ 0.001) for both drug forms when compared to that of placebo. Placebo produced only a slight increase (not significant) with both the oral and i.v. groups. The data show that both oral and i.v. papaverine are equally effective in increasing rCBF in normal subjects.


1980 ◽  
Vol 59 (s6) ◽  
pp. 133s-135s ◽  
Author(s):  
S. L. Swartz ◽  
G. H. Williams ◽  
N. K. Hollenberg ◽  
F. R. Crantz ◽  
L. Levine ◽  
...  

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.


1973 ◽  
Vol 72 (3) ◽  
pp. 615-624 ◽  
Author(s):  
W. Maurer ◽  
U. Volkwein ◽  
J. Tamm

ABSTRACT HCG was infused intravenously into normal male subjects. The doses administered were 500, 100 and 50 IU, respectively. During the initial phase of the infusions the plasma testosterone (T) levels decreased. Thirty minutes after starting the infusion of 500 and 100 IU HCG, respectively, the plasma testosterone increased. Significantly elevated values were observed 60 to 180 minutes after the cessation of HCG administration. The dihydrotestosterone (DHT) concentrations in the plasma showed a varying pattern. On the average this steroid also exhibited an increase in plasma following the HCG administration. From the results no conclusions can be drawn as to the extent to which the plasma concentrations of DHT have been influenced by a secretion from the testes or by a peripheral conversion of T into DHT.


1988 ◽  
Vol 75 (1) ◽  
pp. 85-92 ◽  
Author(s):  
A. R. Scott ◽  
T. Bennett ◽  
I. A. MacDonald

1. Two experiments were carried out. The first with five normal male subjects was placebo controlled and single blind, each subject being studied on two occasions. Lower body subatmospheric pressure (LBSP) was used to assess the cardiovascular effects of graded hypovolaemia before and during either a hyperinsulinaemic, euglycaemic clamp or a placebo clamp using 0.9% (w/v) NaCl only. 2. During hyperinsulinaemia, resting systolic blood pressure rose and was accompanied by forearm vasodilatation. Forearm blood flow (FABF) and heart rate (HR) were higher at each level of LBSP during than before hyperinsulinaemia. In addition, hyperinsulinaemia was accompanied by a small increase in noradrenaline, but packed cell volume did not change. 3. In the second experiment, the effects of a hyperinsulinaemic euglycaemic clamp on the cardiovascular responses to LBSP were assessed in seven diabetic subjects with peripheral and autonomic neuropathy. 4. In contrast to the normal subjects, there was a slight fall in systolic blood pressure during the clamp but no effect was noted on HR or FABF. Mean arterial blood pressure was lower at each level of LBSP during hyperinsulinaemia compared with the pre-elamp period. Packed cell volume fell during the clamp and plasma noradrenaline rose. In one of the diabetic subjects, a precipitous fall in blood pressure occurred during hyperinsulinaemia when LBSP of 10 mmHg (1.3 kPa) was applied, this manoeuvre having been well tolerated before the clamp. 5. The mode of action of hyperinsulinaemia is not clear, but there was, however, no evidence that a fall in plasma volume had occurred.


1987 ◽  
Vol 112 (1) ◽  
pp. 145-150 ◽  
Author(s):  
S. Al-Damluji ◽  
D. Cunnah ◽  
A. Grossman ◽  
L. Perry ◽  
G. Ross ◽  
...  

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


PEDIATRICS ◽  
1957 ◽  
Vol 19 (4) ◽  
pp. 566-579
Author(s):  
C. William Daeschner ◽  
John H. Moyer ◽  
William R. Bell ◽  
John L. Clark

Parenteral administration of reserpine has been evaluated for its antihypertensive effect in normal subjects, in patients with hypertension due to acute nephritis and in a limited number of patients with hypertension due to chronic nephritis. The greatest reduction in blood pressure was obtained in the patients with severe hypertension (diastolic 130 mm of mercury or greater) due to acute nephritis while patients with mild hypertension (diastolic blood pressure less than 110 mm of mercury) showed a less marked response. This has led to the designation of reserpine administered parenterally as an antihypertensive rather than a hypotensive agent. Reserpine appears to be safe and effective for use in the hypertension associated with acute nephritis when given parenterally in doses of 80 to 150 µg/kg of body weight. In certain patients the hypertension is resistant to parenteral administration of reserpine and the addition of hydralazine may be necessary for ideal control of blood pressure. In our experience only rare patients have required combined drug therapy. Patients with chronic nephritis and hypertension show a decrease in blood pressure with reserpine either parenterally or orally. However, in some patients the addition of a ganglionic blocking agent may be necessary to achieve ideal control of the patient's hypertension. Renal hemodynamic studies show a decrease in renal function associated with acute reduction in blood pressure. This decrease is not marked and within an hour is usually followed by a gradual return of renal function toward normal.


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