Bradykinin and renal function in normal man: effects of adrenergic blockade

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.

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.


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.


Perfusion ◽  
2005 ◽  
Vol 20 (5) ◽  
pp. 255-262 ◽  
Author(s):  
Stephen Allen ◽  
William T McBride ◽  
Ian S Young ◽  
Simon W MacGowan ◽  
Terence J McMurray ◽  
...  

Biocompatible cardiopulmonary bypass (CPB) circuits aim to reduce contact activation and its physiological consequences. We investigated the hypothesis that use of Surface Modifying Additive (SMA)-treated circuits (Sorin Group Ltd) compared with non-SMA circuits would be associated with preservation of blood pressure during CPB and modulation of perioperative subclinical renal function (urinary α-1-microglobulin (α-1-m)) and plasma and urinary cytokine changes. In a study of low-risk CABG patients ( n=40), randomized to SMA ( n=20) versus non-SMA circuits ( n=20), we found better preserved blood pressure at CPB initiation in SMA patients (p <0.05), particularly in ACE-inhibited SMA patients ( n=11) versus ACE-inhibited non-SMA patients ( n=10) (p <0.05). Plasma anti-inflammatory IL-10, as well as urinary α-1-m, were elevated 48 hours postoperatively (p <0.05). SMA patients also had lower blood loss (p <0.05). SMA circuits have some clinical benefit, especially in ACE-inhibited patients.


1973 ◽  
Vol 45 (6) ◽  
pp. 733-742 ◽  
Author(s):  
N. K. Hollenberg ◽  
D. F. Adams ◽  
P. Mendell ◽  
H. L. Abrams ◽  
J. P. Merrill

1. The renal vascular response to intravenously administered dopamine was assessed in normal man by selective renal arteriography and xenon washout. Infusion of 3 μg min−1 kg−1 induced renal vasodilatation with an increase in the cortical component of blood flow. Arterial blood pressure was not influenced and a systemic effect was not demonstrable. Lower doses did not induce a renal response. Increasing dosage raised arterial blood pressure and induced subjective symptoms, but did not result in a further increase in renal blood flow. 2. Renal vascular resistance increased with increasing age in the normal subjects. A significant inverse relationship was found between the initial vascular resistance and the renal vasodilator response to dopamine. It thus appears that the vascular effects of increasing age (nephrosclerosis) may limit the dilator response to dopamine. 3. It is concluded that dopamine is an effective renal cortical vasodilator when administered intravenously at doses which are free from other systemic cardiovascular effects. The dose-response relationship must be considered in attempts at reversal of conditions characterized by renal vasoconstriction.


1987 ◽  
Vol 5 (4) ◽  
pp. 425???434 ◽  
Author(s):  
John M.C. Connell ◽  
Judith A. Whitworth ◽  
David L. Davies ◽  
Anthony F. Lever ◽  
A. Mark Richards ◽  
...  

1985 ◽  
Vol 248 (4) ◽  
pp. R400-R406 ◽  
Author(s):  
J. D. Best ◽  
J. B. Halter

To determine whether a reflex increase of sympathetic nervous system activity contributes to maintenance of blood pressure during acute beta-adrenergic blockade, we measured plasma norepinephrine levels and norepinephrine kinetics during propranolol administration. During a 90-min infusion of propranolol (10 mg iv + 80 micrograms/min) in 12 normal subjects, heart rate fell from 56 +/- 2 to 49 +/- 2 (SE) beats/min (P less than 0.001), but there was no fall in mean arterial blood pressure (84 +/- 3 mmHg before and 86 +/- 3 mmHg after propranolol). Arterial plasma norepinephrine levels rose from 183 +/- 20 to 250 +/- 29 pg/ml during propranolol (P less than 0.001), suggesting increased sympathetic vasoconstrictor tone. However, isotope dilution studies using tritiated norepinephrine infusion showed that arterial plasma levels of tritiated norepinephrine rose from 743 +/- 78 to 1,002 +/- 101 dpm/ml during propranolol (P less than 0.001), indicating a reduction in the rate of norepinephrine clearance from plasma. The calculated fall in clearance from 1.90 +/- 0.13 to 1.42 +/- 0.11 1/min (P less than 0.001) entirely accounted for the rise in plasma norepinephrine, since the calculated rate of norepinephrine spillover into plasma remained at the base-line level of 340 +/- 40 ng/min during propranolol. In control studies on four subjects, arterial plasma norepinephrine levels and norepinephrine kinetics did not change from base line during the control period. We conclude that maintenance of blood pressure during propranolol infusion is not due to a reflex generalized increase of sympathetic vasoconstrictor tone.


2001 ◽  
Vol 72 (5) ◽  
pp. 774-775 ◽  
Author(s):  
R. W. G. Johnson ◽  
H. Kreis ◽  
R. Oberbauer ◽  
C. Brattstr??m ◽  
K. Claesson ◽  
...  

2007 ◽  
Vol 177 (4S) ◽  
pp. 411-412
Author(s):  
Javier Miller ◽  
Angela Smith ◽  
Kris Gunn ◽  
Erik Kouba ◽  
Eric M. Wallen ◽  
...  

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