Effect of indapamide on renal plasma flow, glomerular filtration rate and arginine vasopressin in plasma in essential hypertension

1984 ◽  
Vol 26 (5) ◽  
pp. 543-547 ◽  
Author(s):  
E. B. Pedersen ◽  
H. Danielsen ◽  
E. S. Spencer
Keyword(s):  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Arginine Vasopressin ◽  
Filtration Rate ◽  
Renal Plasma Flow

Altered renal response to enhanced endogenous 5-hydroxytryptamine after tryptophan administration in essential hypertension

1992 ◽  
Vol 82 (5) ◽  
pp. 551-557 ◽  
Author(s):  
Fumihiro Tomoda ◽  
Masanobu Takata ◽  
Shinya Oh-Hashi ◽  
Hitoshi Ueno ◽  
Kotaro Yasumoto ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Urinary Excretion ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Renal Response ◽  
Hypertensive Group ◽  
Normotensive Subjects

1. To examine the pathophysiological significance of 5-hydroxytryptamine (serotonin) in essential hypertension, we compared the renal response to intrarenally formed 5-hydroxytryptamine by oral dosing with its precursor, L-tryptophan (2 g), in nine patients with essential hypertension and in six subjects with normotension. 2. Before tryptophan administration, urinary excretion of 5-hydroxytryptamine was significantly higher in the hypertensive group than in the normotensive group (66 ± 8 versus 36 ± 6 ng/min, P < 0.05), whereas renal plasma flow and glomerular filtration rate did not differ between the two groups. After dosing with tryptophan, urinary excretion of 5-hydroxytryptamine significantly increased to the same plateau level in both groups (366 ± 55 ng/min in the hypertensive group and 365 ± 64 ng/min in the normotensive group). Significant and equivalent decreases in renal plasma flow were observed in the early phase after tryptophan administration in both groups (−8.5 ± 3.4% in the hypertensive group and −8.2 ± 1.7% in the normotensive group). Thereafter, renal plasma flow increased to above the baseline value in normotensive subjects, whereas this late vasodilatation was absent in the hypertensive group. Glomerular filtration rate significantly decreased at the time of the fall in renal plasma flow in the normotensive group (106.8 ± 7.8 to 92.7 ± 8.5 ml min−1 1.73 m−2, P < 0.05), whereas it remained unchanged in the hypertensive group (108.2 ± 6.2 to 110.4 ± 6.3 ml min−1 1.73 m−2, not significant). Consequently, the filtration fraction did not change in normotensive subjects (0.21 ± 0.01 versus 0.19 ± 0.01, not significant), but it increased significantly in the hypertensive group (0.22 ± 0.01 versus 0.26 ± 0.02, P < 0.05). A similar sustained antidiuresis was also observed after tryptophan administration in both groups. In addition, the above-described renal functional changes were not accompanied by any significant changes in systemic blood pressure, the renin-angiotensin-aldosterone system, adrenergic activity or plasma 5-hydroxytryptamine concentration in either group. 3. Our data show that in essential hypertension there is a baseline overproduction of renal 5-hydroxytryptamine, which may contribute to a reduction in renal excretory capability. The altered renal response to tryptophan found in essential hypertension may be partly related to the exaggerated efferent arteriolar constriction induced by endogenously formed 5-hydroxytryptamine.

Clinical Renal Function Testing by External Double Isotope Monitoring Technique

1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Correlation Coefficients ◽  
Feedback System ◽  
Effective Renal Plasma Flow ◽  
Advantages And Disadvantages

SummaryAn accurate catheter-free technique for clinical determination simultaneouslyof glomerular filtration rate and effective renal plasma flow by means of radioisotopes has been developed. The renal function is estimated by the amount of radioisotopes necessary to maintain a constant concentration in the patient’s blood. The infusion pumps are steered by a feedback system, the pumps being automatically turned on when the radiation measured over the patient’s head falls below a certain preset level and turned off when this level is again readied. 131I-iodopyracet was used for the estimation of effective renal plasma flow and125I-iothalamate estimation of the glomerular filtration rate. These clearances were compared to the conventional bladder clearances and good correlation was found between these two clearance methods (correlation coefficients 0.97 and.90 respectively). The advantages and disadvantages of this new clearance technique are discussed.

Influence of nifedipine on cyclosporin A nephrotoxicity after unilateral nephrectomy in the spontaneously hypertensive rat

1991 ◽  
Vol 81 (2) ◽  
pp. 271-279 ◽  
Author(s):  
P. G. McNally ◽  
F. Baker ◽  
N. Mistry ◽  
J. Walls ◽  
J. Feehally
Keyword(s):  
Body Weight ◽  
Glomerular Filtration Rate ◽  
Renal Impairment ◽  
Cyclosporin A ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Spontaneously Hypertensive

1. Nifedipine ameliorates cyclosporin A-induced renal impairment in surgically intact (two-kidney) rats. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in spontaneously hypertensive rats after either uninephrectomy or uninephrectomy with contralateral renal denervation. 2. Fourteen days after uninephrectomy pair-fed rats were injected for 14 days with cyclosporin A (25 mg/kg body weight) via the subcutaneous route and with nifedipine (0.1 mg/kg body weight) via the intraperitoneal route. Renal and systemic haemodynamics were measured in conscious unrestrained rats. 3. Whole-blood levels of cyclosporin A did not differ between groups (overall 352 ± 22 ng/ml, means ± sem). After uninephrectomy, cyclosporin A decreased the glomerular filtration rate (olive oil versus cyclosporin A: 0.96 ± 0.04 versus 0.70 ± 0.06 ml min−1 100 g body weight, P < 0.02) and effective renal plasma flow (1.94 ± 0.10 versus 1.38 ± 0.13, P < 0.01), and increased renal vascular resistance {(20.2 ± 1.8) × 104 versus (31.6 ± 3.3) × 104 kPa l−1 s [(20.2 ± 1.8) × 103 versus (31.6 ± 3.3) × 103 dyn s cm−5], P < 0.02} and mean arterial pressure (146.7 ± 6.7 versus 167.3 ± 2.9 mmHg, P < 0.05). Neither renal denervation nor nifedipine prevented the reduction in glomerular filtration rate or effective renal plasma flow induced by cyclosporin A. 4. This study infers that the sympathetic nervous system does not play an active role in cyclosporin A nephrotoxicity and demonstrates that the concomitant administration of nifedipine to rats with reduced renal mass does not ameliorate cyclosporin A-induced renal impairment.

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