Glomerular function reserve and sodium sensitivity

Kimura, Genjiro

doi:10.1007/s10157-005-0353-z

Cited by 20 publications

(14 citation statements)

References 160 publications

(156 reference statements)

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“…Glomerular hypertension is considered to be a risk factor for glomerular damage, 2) and the ACE inhibitor imidapril, which has an efferent arteriolar dilating action, is thought to be useful in that they provide a kidney protective effect. 34) Recently, in Japan, it has been shown that cilnidipine decreased urinary protein in CKD patients.…”

Section: Discussionmentioning

confidence: 99%

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Vasodilatory Effect of Cilnidipine, an L-type and N-type Calcium Channel Blocker, on Rat Kidney Glomerular Arterioles

Konno

Kimura

2008

Int. Heart J.

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SUMMARYCilnidipine is a dihydropyridine calcium channel blocker that acts on both L-type and N-type calcium channels.The effects of cilnidipine given intravenously at doses of 2.5, 5.0, and 10 µg/kg were studied using an ex vivo hydronephrosis model in spontaneously hypertensive rats. The effects of nifedipine at a dose of 10 µg/kg were also studied using the same model as a reference.Cilnidipine caused dose-dependent blood pressure reduction and dilatation of the glomerular afferent arterioles; the arteriolar diameter after cilnidipine infusion at 2.5, 5.0, and 10 µg/kg was 101% ± 3%, 112% ± 4%, and 123% ± 6% relative to baseline, respectively. With cilnidipine, dilatation of the efferent arterioles was also observed; it was maximal after 5 to 10 minutes. Five minutes after administration of 2.5, 5.0, and 10 µg/kg of cilnidipine, the efferent arteriolar diameter was 103% ± 2%, 109% ± 4%, and 119% ± 4% of baseline, respectively. This efferent arteriolar dilating action of cilnidipine was abolished after pretreatment with ω-conotoxin, a selective N-type calcium channel blocker. A dose-dependent increase of glomerular blood flow volume was also observed after cilnidipine infusion. Nifedipine, an L-type calcium channel blocker, at a dose of 10 µg/kg reduced systolic blood pressure to a similar extent as cilnidipine at a dose of 10 µg/kg, but only dilated the afferent arterioles and had no significant effect on efferent arterioles.Cilnidipine dilated both the afferent and efferent glomerular arterioles. The efferent arteriolar dilating effect of cilnidipine may be attributed to its inhibition of the N-type calcium channel. (Int Heart J 2008; 49: 723-732)

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Section: Discussionmentioning

confidence: 99%

“…thought to be caused by glomerular damage due to glomerular hypertension, 2,3) which has been observed in salt-sensitive rats and in spontaneously hypertensive rats (SHRs) with persistent hypertension. 4) Intraglomerular pressure is mainly regulated by the afferent and efferent arterioles.…”

mentioning

confidence: 99%

Vasodilatory Effect of Cilnidipine, an L-type and N-type Calcium Channel Blocker, on Rat Kidney Glomerular Arterioles

Konno

Kimura

2008

Int. Heart J.

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“…7,28 BP becomes salt sensitive when the ultrafiltration capability of the glomerulus is reduced, as seen in CKD, or when renal tubular reabsorption of sodium is enhanced, as seen in primary aldosteronism, diabetes mellitus and metabolic syndrome. 7,29 Glomerular filtration rate (GFR) is usually reduced in CKD but enhanced in primary aldosteronism, diabetes mellitus and metabolic syndrome.…”

Section: Salt Sensitivity and Cardiovascular Eventsmentioning

confidence: 99%

“…30,37,38 Salt restriction restored these rhythms from nondipper to dipper patterns. 30,[32][33][34]37 RENAL DYSFUNCTION AND NON-DIPPER CIRCADIAN RHYTHMS Because glomerular filtration capability is one of the major factors determining salt sensitivity, 7,24,28,36 the nocturnal dip in BP may be less pronounced as a function of GFR loss. We recently showed this quantitative relationship in CKD 38,39 and healthy donors after nephrectomy, 40 in both of whom there was an inverse relationship between GFR and the night/day ratio of BP.…”

Section: Salt Sensitivity and Circadian Rhythm Of Blood Pressurementioning

confidence: 99%

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

2010

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In healthy subjects, blood pressure (BP) drops by 10-20% during the night. Conversely, in patients with the salt-sensitive type of hypertension or chronic kidney disease, nighttime BP does not fall, resulting in an atypical pattern of circadian BP rhythm that does not dip. This pattern is referred to as the 'non-dipper' pattern. Loss of renal functional reserve, due to either reduced ultrafiltration capacity or enhanced tubular sodium reabsorption, induces the salt-sensitive type of hypertension. When salt intake is excessive in patients with salt-sensitive hypertension, the defect in sodium excretory capability becomes evident, resulting in elevated BP during the night. This nocturnal hypertension compensates for diminished natriuresis during the daytime and enhances pressure natriuresis during the night. Nocturnal hypertension and the non-dipper pattern of circadian BP rhythm cause cardiovascular events. When excess salt intake is loaded in patients who are in a salt-sensitive state, glomerular capillary pressure is also elevated, resulting in glomerular sclerosis and eventual renal failure. In this way, salt sensitivity and excess salt intake contribute to both cardiovascular and renal damage at the same time. We propose that salt sensitivity of BP and excess salt intake have important roles in the genesis of the cardiorenal connection. Salt sensitivity and circadian rhythm of BP are the keys to understanding the connections between cardiovascular and renal complications.

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“…[2][3][4] Glomerular hypertension is thought to be one of the main causes of hypertensive renal dysfunction. 5,6 Angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers are of specific benefit in retarding the progression of chronic kidney disease. 7,8 These agents control glomerular capillary pressure by dilating the afferent and efferent arterioles.…”

Section: Introductionmentioning

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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Glomerular function reserve and sodium sensitivity

Cited by 20 publications

References 160 publications

Vasodilatory Effect of Cilnidipine, an L-type and N-type Calcium Channel Blocker, on Rat Kidney Glomerular Arterioles

Vasodilatory Effect of Cilnidipine, an L-type and N-type Calcium Channel Blocker, on Rat Kidney Glomerular Arterioles

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

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

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