Enhanced renal sympathetic nerve activity in response to salt loading in rats.

Yamazaki, Hideaki; Yoshimura, Manabu; Kambara, Seiichi; Lee, Li-Chik; Fukuyama, Masaki; Sasaki, Susumu; Takahashi, Hakuo; Takeda, Kazuo; Ijichi, Hamao

doi:10.1253/jcj.50.442

Cited by 10 publications

(2 citation statements)

References 21 publications

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“…30,31 Urinary concentrations of norepinephrine were determined by high-performance liquid chromatography with electrical chemical detection (HPLC-ECD, EP-10; Eicom, Kyoto, Japan). In brief, 6 mol l À1 HCl (1 ml) was added to the 24-h urinary samples to prevent the decomposition of norepinephrine.…”

Section: Measurement Of Urinary Norepinephrine Excretionmentioning

confidence: 99%

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

et al. 2011

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Cilnidipine, an N/L-type calcium channel blocker, has been reported to inhibit sympathetic nerve activity and has a greater renoprotective effect than L-type calcium channel blockers. To investigate the hypothesis that cilnidipine might ameliorate advanced hypertensive nephropathy and inhibit the renal renin-angiotensin-aldosterone system, cilnidipine (1 mg per kg per day) or amlodipine (1 mg per kg per day) was administered to uninephrectomized deoxycorticosterone (DOCA)-salt hypertensive rats (DOCA-salt) for 4 weeks by gavage. Although the blood pressure in the DOCA-salt group was higher than that of control, neither cilnidipine nor amlodipine had any effect on the increase in blood pressure in the DOCA-salt group. The DOCA (40 mg per kg per week, subcutaneously (s.c.)) and salt (1% NaCl in drinking water) treatment significantly aggravated the levels of urinary protein excretion and creatinine clearance and increased glomerulosclerosis and collagen deposition in the tubulointerstitial area of the kidney. These effects were attenuated by cilnidipine treatment. Reverse transcription-polymerase chain reaction analysis revealed that the renal expression of mRNA for collagen I/IV and transforming growth factor-b was enhanced in the DOCA-salt group and that the overexpression of these molecules was suppressed by cilnidipine. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived superoxide production in the kidney and urinary norepinephrine excretion, which were enhanced in the DOCA-salt group, were suppressed by cilnidipine. Cilnidipine also decreased the activity and expression of angiotensin-converting enzyme (ACE) and the aldosterone concentration in the renal homogenate. Although neither cilnidipine nor amlodipine had any effect on the increased blood pressure in the DOCA-salt group, these renal changes were not induced by treatment with amlodipine. In conclusion, cilnidipine inhibited renal dysfunction, sympathetic nerve activity and renal renin-angiotensin-aldosterone system in the DOCA-salt group.

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Section: Measurement Of Urinary Norepinephrine Excretionmentioning

confidence: 99%

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

et al. 2011

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“…Sodium sensitivity is affected by such factors as defects in renal sodium excretion (37), abnormally weak suppression of intrarenal renin release (38), paradoxical decrease in atrial natriuretic peptide secretion (39), and decreased renal-kallikrein activity (40). Moreover, increased sympathetic nervous system activity (12,13,41) and pressor reactivity (42) may play a large role in this phenomenon. On the other hand, Grassi et al (43) reported that moderate dietary sodium restriction triggers sympathetic activation, and Minami et al (44) also reported that a high-sodium diet decreased LF/HF in non-sodium-sensitive hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%