Interrelationships between sodium clearance, plasma aldosterone, plasma renin activity, renal hemodynamics and blood pressure in renal disease

1979 ◽  
Vol 57 (23) ◽  
pp. 1273-1285 ◽  
Author(s):  
F. C. Reubi ◽  
P. Weidmann ◽  
Z. Glück
Keyword(s):  
Blood Pressure ◽  
Renal Disease ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renal Hemodynamics ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Clearance

The Effect of Weight Reduction on Blood Pressure, Plasma Renin Activity, and Plasma Aldosterone Levels in Obese Patients

1981 ◽  
Vol 304 (16) ◽  
pp. 930-933 ◽  
Author(s):  
Michael L. Tuck ◽  
James Sowers ◽  
Leslie Dornfeld ◽  
Gary Kledzik ◽  
Morton Maxwell
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Weight Reduction ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Obese Patients ◽  
Pressure Plasma

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

Sodium and Renin in the Hypertension of Early Renal Disease

1978 ◽  
Vol 55 (s4) ◽  
pp. 301s-303s ◽  
Author(s):  
S. F. Wong ◽  
M. I. Mitchell ◽  
V. Robson ◽  
R. Wilkinson
Keyword(s):  
Blood Pressure ◽  
Renal Disease ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Exchangeable Sodium ◽  
Hypertensive Patients ◽  
Body Build ◽  
Activity Response ◽  
Normal Controls

1. Plasma renin activity, response to saralasin and exchangeable sodium have been measured in 43 patients with early renal disease. 2. Blood pressure was directly proportional to plasma renin activity. However, mean plasma renin activity was lower in patients with renal disease than in normal controls. 3. Blood pressure fell in response to saralasin infusion in proportion to the pre-infusion plasma renin activity. 4. Exchangeable sodium in hypertensive patients with renal disease did not exceed that in normotensive patients in contrast to earlier reports. Discrepancies may arise from the difficulty in interpreting measured exchangeable sodium in relation to body build.

Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Concurrent Administration ◽  
Angiotensin System

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

1981 ◽  
Vol 60 (4) ◽  
pp. 399-404 ◽  
Author(s):  
C. J. Mathias ◽  
H. L. Frankel ◽  
I. B. Davies ◽  
V. H. T. James ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Diastolic Blood Pressure ◽  
Pressor Response ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sympathetic Stimulation

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

Effect of Acute Volume Depletion on Blood Pressure, Plasma Renin Activity and Plasma Aldosterone Concentration in Hypertensive Subjects

1975 ◽  
Vol 39 (5) ◽  
pp. 545-549
Author(s):  
KENSHI KUMAMOTO ◽  
YOSHITAKA YAMAMOTO ◽  
TERUKAZU KAWASAKI ◽  
TERUO OMAE ◽  
KENJIRO TANAKA
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Volume Depletion ◽  
Plasma Aldosterone Concentration ◽  
Pressure Plasma

Adenovirus-mediated human prostasin gene delivery is linked to increased aldosterone production and hypertension in rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1031-R1036 ◽  
Author(s):  
Cindy Wang ◽  
Julie Chao ◽  
Lee Chao
Keyword(s):  
Blood Pressure ◽  
Gene Transfer ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Aldosterone Production ◽  
Renal Kallikrein

Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, and aorta, and immunoreactive human prostasin was detected in the circulation and urine of rats receiving prostasin gene transfer. A single injection of adenovirus carrying the prostasin gene caused prolonged increases in blood pressure for 3–4 wk. Blood pressure increase was accompanied by elevated plasma aldosterone levels and reduced plasma renin activity. The increase in blood pressure and plasma aldosterone levels as well as the reduction of plasma renin activity correlated with the expression of human prostasin transgene. Elevated plasma aldosterone levels were detected at 3 days after gene transfer before the development of hypertension, indicating that stimulation of mineralocorticoid production is the primary target of prostasin. Prostasin gene transfer significantly reduced urinary K+ excretion but increased urinary Na+ and kallikrein excretion. Elevated renal kallikrein levels promote natriuresis, which may lead to sodium escape and prevent further increases of blood pressure after prostasin gene transfer. In summary, these results suggest that prostasin participates in blood pressure and electrolyte homeostasis by regulating the renin-angiotensin-aldosterone and kallikrein-kinin systems.

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