scholarly journals Effect of nitric oxide on exercise-induced proteinuria in rats

2003 ◽  
Vol 95 (5) ◽  
pp. 1867-1872 ◽  
Author(s):  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Ümit Kemal Şentürk
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Mixed Type ◽  
Channel Blocker ◽  
Renal Hemodynamics ◽  
Urinary Protein ◽  
Exhaustive Exercise ◽  
No Donor ◽  
Protein Levels

Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nω-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.

scholarly journals Anti-Hypertensive Drugs and Sexual Dysfunction in Men

2020 ◽  
Vol 13 (01) ◽  
pp. 1-11
Author(s):  
Noverio Tarukallo ◽  
Haerani Rasyid
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Sexual Dysfunction ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Angiotensin Receptor Blocker ◽  
Ace Inhibitor ◽  
Channel Blocker ◽  
Angiotensin Receptor ◽  
Β Blocker

Salah satu faktor yang memiliki risiko yang terkait dengan kejadian disfungsi seksual pada pria adalah obat anti-hipertensi. Obat anti-hipertensi yang memiliki efek menyebabkan disfungsi seksual pada pria termasuk; diuretik, Clonidine, dan β-blocker (kecuali nebivolol), tetapi ada beberapa obat anti-hipertensi yang memiliki efek netral, bahkan memiliki efek positif yang dalam hal ini dapat meningkatkan fungsi seksual pada pria. Obat anti-hipertensi yang memiliki efek netral pada fungsi seksual pria meliputi; Calcium Channel Blocker dan ACE-Inhibitor dan yang memiliki efek meningkatkan fungsi seksual pada pria termasuk; ARB dan β-blocker yaitu nebivolol. Penggunaan obat anti-hipertensi dapat mempengaruhi fungsi seksual pada pria melalui mekanisme yang berbeda. Obat anti-hipertensi seperti diuretik, β-blocker, dan clonidine dapat menyebabkan disfungsi seksual pada pria melalui mekanisme perubahan dalam aliran simpatis, efek pada kontraksi otot polos fisik, dan melalui pengaruh pada kadar hormon androgen. Angiotensin Receptor Blocker dan Nebivolol dapat meningkatkan fungsi seksual melalui mekanisme penghambatan pada Angiotensin II dan meningkatkan bioavailabilitas Nitric Oxide.

scholarly journals Effect of Salt-loading and Calcium Channel Blocker on Renal Hemodynamics

1994 ◽  
Vol 35 (4) ◽  
pp. 512-512
Author(s):  
Tatsuo Shimosawa ◽  
Katsuyuki Ando ◽  
Toshiro Fujita
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Renal Hemodynamics ◽  
Salt Loading

Successful use of calcium channel blocker for management of arterio-venous malformations following Fontan procedure

2018 ◽  
Vol 28 (12) ◽  
pp. 1468-1470
Author(s):  
Ramzi Hamzeh ◽  
Ziad Bulbul ◽  
Jana Assy
Keyword(s):  
Nitric Oxide ◽  
Arteriovenous Malformation ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Calcium Channel Blockers ◽  
Pulmonary Circulation ◽  
Channel Blocker ◽  
Fontan Procedure ◽  
Channel Blockers ◽  
Venous Malformations

AbstractIn diffuse forms of arteriovenous malformation following Fontan procedure, “classical” medical therapy, inhaled nitric oxide and sildenafil, may play a role, until re-direction of hepatic flow to pulmonary circulation cures it. However, in refractory cases, as reported in our 2-year-old patient, unusual medications such as calcium channel blockers can be tried and continued if patients respond adequately.

scholarly journals Protective Actions of Cilnidipine: Dual L/N-Type Calcium Channel Blocker Against Hypertensive Renal Injury in Rats

2021 ◽  
Vol 14 (4) ◽  
pp. 1887-1893
Author(s):  
Gouher Banu Shaikh ◽  
Surekha Hippargi ◽  
Dewan S. A Majid ◽  
Kusal K Das
Keyword(s):  
Angiotensin Ii ◽  
Calcium Channels ◽  
Creatinine Clearance ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Renal Injury ◽  
Channel Blocker ◽  
Urinary Protein ◽  
Fourth Generation ◽  
Animal House

Background: Cilnidipine belongs to fourth generation dihydropyridine calcium channel blocker (CCB). It is a dual L & N-type CCB. L- type calcium channels are present on the vascular smooth muscle and N-type calcium channels are present on the presynaptic nerve terminals. Cilnidipine has a vasodilating effect, its action is slow and long lasting. Aim and objectives: Aim of present study was to demonstrate the beneficial effects of cilnidipine on the hypertensive renal injury rats. And our objectives is to assess renal injury parameters (Proteinuria, Creatinine clearance, Renal fibrosis/glomerulosclerosis) in response to chronic NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) treatment in the presence or absence of cilnidipine treatment. Material and methods: Male albino Wister rats were procured from institutional animal house, divided into 4 groups (n=6 in each group). Group1 treated with vehicle (control), group2 treated with cilnidipine, group3 treated with L-NAME, group4 treated with L-NAME & cilnidipine. 24 hour urinary protein and creatinine clearance were measured. Serum urea and creatinine levels are also measured. Urinary and serum Angiotensin II levels were measured. Histopathological examination of kidneys was performed. Results: Our results demonstrate that treatment with cilnidipine (group4) there is reduction in 24hr urinary protein, improvement in creatinine clearance. We observed there was renal glomerulosclerosis and tubular degeneration of kidney tubules in group3 rats and reduction of renal injury in group4 rats. We also found reduced urinary and serum Angiotensin II level in cilnidipine treated (group 4) rats. Conclusion: These findings indicated that cilnidipine act as renoprotective agent and reduces glomerular damage in L-NAME induced hypertensive rats.

Pranidipine, a 1,4-Dihydropyridine Calcium Channel Blocker that Enhances Nitric Oxide-Induced Vascular Relaxation

2006 ◽  
Vol 19 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Toyoki Mori ◽  
Hiromichi Takase ◽  
Kiyotaka Toide ◽  
Takahiro Hirano ◽  
Toshimi Kambe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Vascular Relaxation ◽  
Dihydropyridine Calcium Channel Blocker

CGRP Modulates Orofacial Pain through Mediating Neuron-Glia Crosstalk

2020 ◽  
Vol 100 (1) ◽  
pp. 98-105
Author(s):  
H. Liang ◽  
H. Hu ◽  
D. Shan ◽  
J. Lyu ◽  
X. Yan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Signaling Pathway ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Orofacial Pain ◽  
Nitric Oxide Donor ◽  
Satellite Glial Cells ◽  
Trigeminal Neurons ◽  
Gene And Protein Expression

Calcitonin gene-related peptide (CGRP) plays a crucial role in the modulation of orofacial pain, and we hypothesized that CGRP mediated a neuron-glia crosstalk in orofacial pain. The objective of this study was to elucidate the mechanisms whereby CGRP mediated trigeminal neuron-glia crosstalk in modulating orofacial pain. Orofacial pain was elicited by ligating closed-coil springs between incisors and molars. Trigeminal neurons and satellite glial cells (SGCs) were cultured for mechanistic exploration. Gene and protein expression were determined through immunostaining, polymerase chain reaction, and Western blot. Orofacial pain was evaluated through the rat grimace scale. Our results revealed that the expressions of CGRP were elevated in both trigeminal neurons and SGCs following the induction of orofacial pain. Intraganglionic administration of CGRP and olcegepant exacerbated and alleviated orofacial pain, respectively. The knockdown of CGRP through viral vector-mediated RNA interference was able to downregulate CGRP expressions in both neurons and SGCs and to alleviate orofacial pain. CGRP upregulated the expression of inducible nitric oxide synthase through the p38 signaling pathway in cultured SGCs. In turn, L-arginine (nitric oxide donor) was able to enhance orofacial pain by upregulating CGRP expressions in vivo. In cultured trigeminal neurons, L-arginine upregulated the expression of CGRP, and this effect was diminished by cilnidipine (N-type calcium channel blocker) while not by mibefradil (L-type calcium channel blocker). In conclusion, CGRP modulated orofacial pain through upregulating the expression of nitric oxide through the p38 signaling pathway in SGCs, and the resulting nitric oxide in turn stimulated CGRP expression through N-type calcium channel in neurons, building a CGRP-mediated positive-feedback neuron-glia crosstalk.

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