Effect of verapamil on renal plasma flow, glomerular filtration rate and plasma angiotensin II, aldosterone and arginine vasopressin in essential hypertension

1985 ◽  
Vol 29 (3) ◽  
pp. 257-261 ◽  
Author(s):  
S. S. S�rensen ◽  
O. �. Thomsen ◽  
H. Danielsen ◽  
E. B. Pedersen
1988 ◽  
Vol 255 (3) ◽  
pp. F545-F551
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey

The mechanism by which atrial natriuretic peptide (ANP) increases renal water and solute excretion is not fully understood. We studied the renal effects of ANP and angiotensin II (ANG II) separately and together in uninephrectomized conscious dogs (n = 7) in sodium metabolic balance (80 meq/day). Exogenous ANG II and ANP were without measurable systemic effects as demonstrated by absence of changes in blood pressure, plasma aldosterone concentration, and plasma renin activity. The quantity of ANG II that had significant renal effects that were without measurable systemic effects was 0.2 pmol.kg-1.min-1. Three infusion rates of ANP had significant renal effects (1, 10, and 20 pmol.kg-1.min-1). These quantities of ANP caused significant diuresis, natriuresis, kaliuresis, and increased glomerular filtration rate without significant changes in renal plasma flow. ANG II alone caused significant antidiuresis, antinatriuresis, and decreased glomerular filtration rate and renal plasma flow. When ANG II and ANP were given together, no change in urinary flow rate, urinary sodium or potassium excretion, or renal plasma flow was observed, whereas glomerular filtration rate increased. Filtration fraction increased significantly with ANG II and ANP separately and together. Intrarenal ANP prevents the ANG II-induced decrement in urinary sodium excretion and urine flow rate. ANP may play an important role in escape from the sodium-retaining action of intrarenal ANG II.


1991 ◽  
Vol 80 (2) ◽  
pp. 143-147 ◽  
Author(s):  
Luis M. Villamediana ◽  
Mercedes Velo ◽  
Ana Olivera ◽  
Luis Hernando ◽  
Carlos Caramelo ◽  
...  

1. The effects of angiotensin II on glomerular filtration rate and renal plasma flow were studied in surgically instrumented conscious control and cirrhotic rats. In addition, angiotensin II binding and the contractile response to angiotensin II were studied in glomeruli isolated from cirrhotic and control rats. 2. Cirrhotic rats had a higher glomerular filtration rate and a higher renal plasma flow than control animals. A non-pressor dose of angiotensin II induced small but significant decreases in glomerular filtration rate and renal plasma flow in both control and cirrhotic rats, the effect on renal plasma flow being the most pronounced. 3. Plasma renin and aldosterone concentrations were similar in control and cirrhotic rats. 4. The cross-sectional area of glomeruli from cirrhotic rats was 42% greater than that of glomeruli from control animals. Angiotensin II (10−9 mol/l) decreased the cross-sectional area of glomeruli from control animals by 6.4 ± 0.9% and of glomeruli from cirrhotic rats by 6.6 ± 0.8% (P = not significant for comparison between control and cirrhotic animals). 5. There were no differences between control and cirrhotic rats in the affinity of angiotensin II for its glomerular receptors. However, the angiotensin II receptor density was higher in cirrhotic than in control rats, thereby producing an increased total angiotensin II binding in cirrhotic rats. 6. Since no functional differences between control and cirrhotic animals were present in the response to angiotensin II, even though angiotensin II binding was increased, a post-receptor blockade of the angiotensin II signal could be present in cirrhotic rats.


1992 ◽  
Vol 82 (5) ◽  
pp. 551-557 ◽  
Author(s):  
Fumihiro Tomoda ◽  
Masanobu Takata ◽  
Shinya Oh-Hashi ◽  
Hitoshi Ueno ◽  
Kotaro Yasumoto ◽  
...  

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.


2010 ◽  
Vol 63 (9-10) ◽  
pp. 630-637
Author(s):  
Tamara Dragovic ◽  
Boris Ajdinovic ◽  
Vesna Ilic ◽  
Zvonko Magic ◽  
Zoran Andjelkovic ◽  
...  

Introduction. Our study was aimed at determining whether the polymorphism of genes for different components of the renin-angiotensin-aldosterone system could influence the renal hemodynamic response to losartan treatment. Material and method. The study included 35 patients with type 1 diabetes mellitus and persistent albuminuria, genotyped for the 1166 A/C polymorphism gene for the angiotensin II type 1 receptor and I/D polymorphism of the angiotensin-converting enzyme gene. The participants were divided into groups according to the combinations of A or C allele: AA, AC, CC; and according to the combinations of I or D allele: II, ID and DD genotype. The patients received losartan therapy for 12 weeks. The renal hemodynamic measurements were determined at baseline and after the examination period. Results. Losartan therapy significantly reduced the filtration fraction from the baseline by 0.018?0.024 (p=0.012) only in the AC genotype. The glomerular filtration rate remained unchanged in all genotype groups. A significant increase in the effective renal plasma flow was obtained only in AC genotype (544?88 vs 575?90ml/min; p=0.02), while significant reductions in the renal vascular resistance were found in AA group (115?25 vs 95?21 mmHgx1-1xmin-1; p=0.001) and in AC group (118?30 vs 101?28 mmHgx1-1xmin-1; p=0.001). A significant reduction of the glomerular filtration rate by 8?10 ml/min was obtained only in the DD genotype (p=0.016), and only the DD genotype achieved a significant reduction of the filtration fraction by 0.019?0,022 (p=0.008). The most pronounced increase of the effective renal plasma flow was found only in the ID genotype (536 ?75 vs 591?63 ml/min; p=0.01). The reduction of the renal vascular resistance was independent of ACE gene polymorphism. Conclusion. Our study shows that individual renal vascular response to losartan treatment in diabetic patients with persistent albuminuria, could be influenced by genetic polymorphisms.


1994 ◽  
Vol 267 (6) ◽  
pp. R1472-R1478 ◽  
Author(s):  
A. M. Alberola ◽  
F. J. Salazar ◽  
T. Nakamura ◽  
J. P. Granger

Recent in vitro studies have provided evidence that the vasoconstrictor actions of angiotensin II on afferent arterioles are enhanced by nitric oxide synthesis inhibition. Although these studies suggest that nitric oxide may play a role in protecting the afferent arterioles from angiotensin II-induced vasoconstriction, the importance of this interaction in the regulation of glomerular filtration rate and renal blood flow in the intact, conscious animal is not known. The objective of the present study was to determine the role of nitric oxide in modulating the renal hemodynamic and excretory effects of angiotensin II. Angiotensin II was infused at rates of 0.5, 1.0, and 2.0 micrograms.kg-1.min-1 intrarenally in conscious, chronically instrumented dogs in both the presence and absence of nitric oxide synthesis inhibition by continuous intrarenal infusion of NG-nitro-L-arginine methyl ester (3 micrograms.kg-1.min-1). At a dose of 0.5 micrograms.kg-1.min-1, angiotensin II decreased renal plasma flow by 19%, while having no effect on glomerular filtration rate in control dogs. In contrast, angiotensin II decreased renal plasma flow by 54%, glomerular filtration rate by 40%, and increased renal vascular resistance by 125% in the presence of intrarenal nitric oxide synthesis blockade. At doses of 1.0 and 2.0 micrograms.kg-1.min-1, angiotensin II reduced renal plasma flow by 36 and 45%, glomerular filtration rate by 17 and 23%, and increased renal vascular resistance by 80 and 120%, respectively, in control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)


1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen

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.


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