Cilnidipine Attenuates Renal Nerve Stimulation-Induced Renal Vasoconstriction and Antinatriuresis in Anesthetized Dogs

Takahara, Akira; Dohmoto, Hideki; Hisa, Hiroaki; Satoh, Susumu; Yoshimoto, Ryota

doi:10.1016/s0021-5198(19)31344-7

Cited by 4 publications

(1 citation statement)

References 18 publications

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“…Furthermore, we did not measure urinary glucose excretion and urinary glucose concentration as carried out by Jiman et al [43]. However, the decreases in urinary flow rate and sodium excretion we measured were in agreement with a number of previous studies that described similar responses to LFS [16,[57][58][59][60], which suggests that the absolute reduction in urinary glucose (without a change in glucose concentration) reported by Jiman et al is likely due to these antidiuretic effects [43].…”

Section: Discussionsupporting

confidence: 87%

Effect of Low-Frequency Renal Nerve Stimulation on Renal Glucose Release during Normoglycemia and a Hypoglycemic Clamp in Pigs

Nistor,

Schmidt,

Klingner

et al. 2024

IJMS

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Previously, we demonstrated that renal denervation in pigs reduces renal glucose release during a hypoglycemic episode. In this study we set out to examine changes in side-dependent renal net glucose release (SGN) through unilateral low-frequency stimulation (LFS) of the renal plexus with a pulse generator (2–5 Hz) during normoglycemia (60 min) and insulin-induced hypoglycemia ≤3.5 mmol/L (75 min) in seven pigs. The jugular vein, carotid artery, renal artery and vein, and both ureters were catheterized for measurement purposes, blood pressure management, and drug and fluid infusions. Para-aminohippurate (PAH) and inulin infusions were used to determine side-dependent renal plasma flow (SRP) and glomerular filtration rate (GFR). In a linear mixed model, LFS caused no change in SRP but decreased sodium excretion (p < 0.0001), as well as decreasing GFR during hypoglycemia (p = 0.0176). In a linear mixed model, only hypoglycemic conditions exerted significant effects on SGN (p = 0.001), whereas LFS did not. In a Wilcoxon signed rank exact test, LFS significantly increased SGN (p = 0.03125) and decreased sodium excretion (p = 0.0017) and urinary flow rate (p = 0.0129) when only considering the first instance LFS followed a preceding period of non-stimulation during normoglycemia. To conclude, this study represents, to our knowledge, the first description of an induction of renal gluconeogenesis by LFS.

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Section: Discussionsupporting

confidence: 87%

Effect of Low-Frequency Renal Nerve Stimulation on Renal Glucose Release during Normoglycemia and a Hypoglycemic Clamp in Pigs

Nistor,

Schmidt,

Klingner

et al. 2024

IJMS

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Calcium channel blocker in patients with chronic kidney disease

et al. 2021

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Background Chronic kidney disease (CKD) is involved in a progressive deterioration in renal function over the years and is now a global public health problem. Currently, reducing the number of patients progressing to end-stage renal failure is urgently necessary. Hypertension and CKD interact with each other, and good control of blood pressure (BP) can improve CKD patients’ prognosis. With the current global trend for more strict BP control, the importance of BP management and the need for medication to achieve this strict goal are increasing. Calcium channel blockers (CCBs), which target voltage-dependent calcium channels, are frequently used in combination with renin–angiotensin–aldosterone system inhibitors for CKD patients because of their strong BP-lowering properties and relatively few adverse side effects. Calcium channels have several subtypes, including L, N, T, P/Q, and R, and three types of CCBs, L-type CCBs, L-/T-type CCBs, and L-/N-type CCBs, that are available. Nowadays, the new functions and effects of the CCBs are being elucidated. Conclusion We should use different types of CCBs properly depending on their pharmacological effects, such as the strength of antihypertensive effects and the organ protection effects, taking into account the pathophysiology of the patients. In this article, the role and the use of CCBs in CKD patients are reviewed.

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A new-generation N/L-type calcium channel blocker leads to less activation of the renin–angiotensin system compared with conventional L type calcium channel blocker

Konoshita

Makino

Kimura

et al. 2010

Journal of Hypertension

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Cilnidipine Attenuates Renal Nerve Stimulation-Induced Renal Vasoconstriction and Antinatriuresis in Anesthetized Dogs

Cited by 4 publications

References 18 publications

Effect of Low-Frequency Renal Nerve Stimulation on Renal Glucose Release during Normoglycemia and a Hypoglycemic Clamp in Pigs

Effect of Low-Frequency Renal Nerve Stimulation on Renal Glucose Release during Normoglycemia and a Hypoglycemic Clamp in Pigs

Calcium channel blocker in patients with chronic kidney disease

A new-generation N/L-type calcium channel blocker leads to less activation of the renin–angiotensin system compared with conventional L type calcium channel blocker

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