Natriuretic Response to Head-Out Immersion in Humans with Recent Kidney Transplants

1993 ◽  
Vol 85 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Ton J. Rabelink ◽  
Karin A. van Tilborg ◽  
Ronald J. Hené ◽  
Hein A. Koomans
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Renin Activity ◽  
Control Group ◽  
Control Subjects ◽  
Renal Vascular

1. Recently implanted kidneys may have decreased flexibility to adjust sodium excretion to volume challenges, since modulation by renal sympathetic nerve activity is absent. To examine this hypothesis, we studied the natriuretic response to head-out water immersion in eight patients with well-functioning renal allografts of 37 days (range 24–56 days), at a time when renal re-innervation has probably not occurred. 2. By the third hour of head-out water immersion, sodium excretion had increased equally in the patients (from 120 +21 to 204 +37 μmol/min) and in eight healthy control subjects (from 105 +9 to 191+19 μmol/min). 3. Glomerular filtration rate was 60 + 6 ml/min in the patients and 113 +6 ml/min in the control subjects, and did not change upon head-out water immersion. Estimated renal plasma flow increased upon head-out water immersion in the control group but not in the patients. Blood pressure decreased similarly in both groups. The renal vascular resistance, calculated from these data, decreased in response to head-out water immersion in the control subjects but not in the renal transplant patients. 4. Head-out water immersion suppressed plasma renin activity only in the normal group, whereas the plasma aldosterone level was suppressed in both groups. The natriuretic response in patients was associated with about 3-fold elevated plasma levels of atrial natriuretic peptide. 5. Since renal re-innervation at 37 days after transplantation is very unlikely, these data suggest that inact renal innervation is not mandatory for a normal natriuretic response to head-out water immersion in humans. However, sympathetic modulation might be involved in the decrease in renal vascular resistance and plasma renin activity normally observed during immersion.

Renal Haemodynamics and Plasma Renin in Patients with Essential Hypertension

1976 ◽  
Vol 50 (5) ◽  
pp. 409-414 ◽  
Author(s):  
E. B. Pedersen ◽  
H. J. Kornerup
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Control Group ◽  
Hypertensive Patients ◽  
Control Subjects ◽  
Hypertensive Group ◽  
Renal Vascular

1. Blood pressure, glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured in twenty-three patients with essential hypertension and in twenty-one control subjects. Plasma renin concentration was measured in all the hypertensive patients and in fifteen control subjects. 2. GFR and RPF were similar in the hypertensive group and in the control group, whereas the renal vascular resistance was significantly higher in the hypertensive patients. GFR and RPF decreased with increasing blood pressure in both groups. Increasing age induced a further reduction in GFR and RPF in the control subjects but not in the hypertensive patients. 3. Plasma renin concentration in the hypertensive group did not differ from that in the control subjects. The concentration was not correlated to age in either the hypertensive or normal group. 4. Plasma renin index was positively correlated to GFR and RPF and inversely correlated to filtration fraction and renal vascular resistance. 5. It is concluded that GFR and RPF depend on blood pressure in both hypertensive patients and normotensive control subjects. In contrast to the control group, the age effect was negligible in the hypertensive group. It is suggested that renin release depends on changes in renal vascular resistance in the arterioles at the glomerulus and the results support the baroreceptor theory of renin release.

Altered renal vascular tone and plasma renin activity due to fastigial and baroreceptor activation

1980 ◽  
Vol 239 (2) ◽  
pp. H232-H237
Author(s):  
S. Koyama ◽  
W. S. Ammons ◽  
J. W. Manning
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Carotid Sinus ◽  
Pressor Response ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Renin Activity ◽  
Superior Cerebellar Peduncle ◽  
Renal Vascular ◽  
Sinus Pressure

The effects of stimulating the cerebellar fastigial nucleus in altering renal vascular resistance were assessed at three levels of carotid sinus pressure (CSP). In alpha-chloralose-anesthetized, vagotomized, and salt-depleted cats, renal vascular resistance changes were established by perfusing the isolated carotid sinus at high (197 +/- 17 mmHg), medium (117 +/- 8 mmHg), and low (60 +/- 7 mmHg) pressure. The hemodynamic state of the perfused kidney was determined from flow-pressure curves. In relative units, the flow resistance in the renal bed was for low CSP, 2.60 PRU100, for medium CSP, 2.25 PRU100, and for high CSP, 1.22 PRU100. The fastigial pressor response was imposed at each flow-presure determination with or without superior cerebellar peduncle lesions. An increase in the resistance with the fastigial stimulation was noted at each of the three hemodynamic states; 14% at low, 26% at medium, and 22% at high CSP. With increased renal vascular resistance evoked through the baroreflex, there was an increase in plasma renin activity. The rise in plasma renin activity could be attributed in large part to an increase in sympathetic renal nerve activity wherein the fastigial pressor response shared a synergistic action at medium and high carotid sinus pressure. The effect of the fastigial stimulation on renal vascular resistance and renin secretion was abolished by transections of the superior cerebellar peduncles.

Uranyl Nitrate Acute Renal Failure in the Dog: Early Changes in Renal Function and Haemodynamics

1975 ◽  
Vol 48 (1) ◽  
pp. 9-16 ◽  
Author(s):  
J. G. Kleinman ◽  
J. S. McNeil ◽  
W. Flamenbaum
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Uranyl Nitrate ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Vascular Resistance ◽  
Inulin Clearance ◽  
Renal Vascular

1. Sodium excretion, plasma renin activity (PRA), inulin clearance, total renal blood flow (RBF), renal cortical radiomicrosphere distribution and systemic haemodynamics were examined during the first 3 h after intravenous administration of uranyl nitrate (19.9 μmol/kg body wt.; 10 mg/kg) in the dog. 2. During the 3 h of study after uranyl nitrate, urine flow remained stable or increased, sodium excretion increased approximately fivefold, renal vascular resistance increased threefold, and concordant decreases in RBF and inulin clearance to 40–50% of control values occurred. At 3 h total cortical RBF decreased to 35% of control values and the ratio of blood flow in outer to inner cortical zones also decreased, reflecting outer cortical ischaemia. PRA increased in the first hour after uranyl nitrate and slowly declined thereafter, though not to control values. 3. Respiratory rate, heart rate, mean systemic blood pressure and cardiac output were unchanged after uranyl nitrate, demonstrating that the changes in renal vascular resistance occurred without a change in peripheral vascular resistance. 4. It is postulated that increased renin-angiotensin system activity mediates the change in renal haemodynamics and the consequent fall in glomerular filtration.

Modulation of ANG II receptor and its mRNA in normal rat by low-protein feeding

1994 ◽  
Vol 266 (1) ◽  
pp. F161-F161
Author(s):  
J. E. Benabe ◽  
S. Wang ◽  
J. N. Wilcox ◽  
M. Martinez-Maldonado
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Ang Ii ◽  
The Third ◽  
Low Protein ◽  
Protein Feeding ◽  
Normal Rat ◽  
Renal Vascular

Pages F660–F669: J. E. Benabe, S. Wang, J. N. Wilcox, and M. Martinez-Maldonado. “Modulation of ANG II receptor and its mRNA in normal rat by low-protein feeding.” Page F662, Table 1: for the third group (NP), the value for renal vascular resistance is incorrect and should be 9 ± 1 dyn·s·cm-5; also for the NP group, the plasma renin activity is incorrectly expressed as a negative value and should be 10.1 ± 1.3 ng·ml-1h–1.

Nonpressor mechanisms in CNS-induced natriuresis

1979 ◽  
Vol 237 (2) ◽  
pp. F157-F166 ◽  
Author(s):  
David R. Mouw ◽  
Arthur J. Vander ◽  
Jacques J. Bourgoignie ◽  
Sandra S. Kutschinski ◽  
Nancy P. Mathias
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Renin Activity ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Control Group ◽  
Natriuretic Hormone ◽  
High Sodium ◽  
Time Control

Ventriculocisternal perfusion was performed in pentobarbital-anesthetized dogs. Perfusion of high Na (300 mM NaCl) artificial cerebrospinal fluid (CSF) (E) for 2 h was preceded by 2 h of control (C) and was followed by 2 h of recovery (R) during which normal (150 mM NaCl) artificial CSF was perfused. A time-control group was perfused with normal artificial CSF throughout C, E, and R. High sodium perfusion resulted in a marked natriuresis in each of nine animals and suppression of plasma renin activity. There were no simultaneous changes in mean arterial pressure, glomerular filtration rate, or renal plasma flow. Sodium excretion and plasma renin activity showed a slight gradual rise in the time-control group, but no significant differences were observed between the C and E periods; sodium excretion and plasma renin activity were similar in the high Na and time-control groups during C and R, but significantly different during E. It is concluded that when CSF sodium is elevated by perfusing artificial CSF, the resulting natriuresis and suppression of plasma renin activity are not caused by hemodynamic changes. antidiuretic hormone; natriuretic hormone; renin; renal hemodynamics; cerebrospinal fluid; osmoreceptors; sodium receptors Submitted on July 17, 1978 Accepted on April 10, 1979

Accelerated Hypertension in the Rat: Relation between Renin, Renal Vascular Lesions, Salt Intake and Blood Pressure

1976 ◽  
Vol 51 (s3) ◽  
pp. 69s-71s ◽  
Author(s):  
Sauwaluck Chusilp ◽  
A. S. P. Hua ◽  
Priscilla Kincaid-Smith
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Tap Water ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Control Group ◽  
Group 3 ◽  
Renal Vascular ◽  
Control Group Group

1. Complete ligation of the aorta between the origins of the two renal arteries in the rat produces a predictable form of accelerated hypertension. Changes in the blood pressure, plasma renin activity and renal histological lesions have been studied. 2. Group 1 rats and their control group (group 2) received tap water, and group 3 and its control group (group 4) received sodium chloride solution (0·154 mol/l) in place of tap water, for 4 weeks before aortic ligation. In the experimental groups 1 and 3, complete ligation was carried out. In groups 2 and 4 the aorta and renal arteries were exposed, but not ligated. Interlobular artery lesions were studied on a blind basis and graded 0–4 according to severity. 3. Groups 1 and 3 developed severe hypertension. In group 1 the raised mean arterial pressure showed a significant correlation with increased plasma renin activity. Both mean arterial pressure and plasma renin activity also showed a significant correlation with changes in interlobular arteries. In group 3 the raised mean arterial blood pressure did not show a significant correlation with the depressed plasma renin activity, or with changes in interlobular arteries. A significant correlation was, however, found between plasma renin activity and interlobular artery lesions in group 3. 4. These results suggest that the renin-angiotensin system may influence renal vascular lesions through some mechanism independent of the blood pressure.

scholarly journals Plasma Renin Activity and Sleep-Wake Structure of Narcoleptic Patients and Control Subjects Under Continuous Bedrest

SLEEP ◽  
1992 ◽  
Vol 15 (5) ◽  
pp. 423-429 ◽  
Author(s):  
H. Schulz ◽  
G. Brandenberger ◽  
S. Gudewill ◽  
D. Hasse ◽  
E. Kiss ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Wake Structure ◽  
Control Subjects ◽  
And Control

Effects of blood viscosity on plasma renin activity and renal hemodynamics

1986 ◽  
Vol 250 (1) ◽  
pp. F40-F46 ◽  
Author(s):  
S. Simchon ◽  
R. Y. Chen ◽  
R. D. Carlin ◽  
F. C. Fan ◽  
K. M. Jan ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Blood Viscosity ◽  
Plasma Renin ◽  
Plasma Viscosity ◽  
Renal Hemodynamics ◽  
Renin Activity ◽  
Sodium Pentobarbital ◽  
Coefficient Of Correlation ◽  
Arterial Blood ◽  
Renal Vascular

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

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