ArticleHypertension research : official journal of the Japanese Society of Hypertension2019
Renal nerves contribute to hypertension in Schlager BPH/2J mice.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Cardiorenal syndrome: long road between kidney and heart.Heart failure reviews · 2022Review
- Patient Selection for Renal Denervation in Hypertensive Patients: What Makes a Good Candidate?Vascular health and risk management · 2022Review
- Vascular smooth muscle ion channels in essential hypertension.Frontiers in physiology · 2022Review
- Renal denervation does not affect hypertension or the renin-angiotensin system in a rodent model of juvenile-onset polycystic kidney disease: clinical implications.Scientific reports · 2021Article
- Effect of renal denervation on long-term outcomes in patients with resistant hypertension.Cardiovascular diabetology · 2021Review
- Renal Denervation and Celiac Ganglionectomy Decrease Mean Arterial Pressure Similarly in Genetically Hypertensive Schlager (BPH/2J) Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Article
- Neural suppression of miRNA-181a in the kidney elevates renin expression and exacerbates hypertension in Schlager mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Mechanisms underlying the effects of renal denervation in renovascular hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Mechanisms Responsible for Genetic Hypertension in Schlager BPH/2 Mice.Frontiers in physiology · 2019Review
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10 authors at 4 institutions in 1 country.
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Abstract
Schlager mice (BPH/2J) are hypertensive due to a greater contribution of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS). The kidneys of BPH/2J are hyper-innervated suggesting renal nerves may contribute to the hypertension. We therefore determined the effect of bilateral renal denervation (RD) on hypertension in BPH/2J. Mean arterial pressure (MAP) was measured by radiotelemetry before and for 3 weeks after RD in BPH/2J and BPN/3J. The effects of pentolinium and enalaprilat were examined to determine the contribution of the SNS and RAS, respectively. After 3 weeks, MAP was -10.9 ± 2.1 mmHg lower in RD BPH/2J compared to baseline and -2.1 ± 2.2 mmHg in sham BPH/2J (P < 0.001, n = 8-10). RD had no effect in BPN/3J (P > 0.1). The depressor response to pentolinium was greater in BPH/2J than BPN/3J, but in both cases the response in RD mice was similar to sham. Enalaprilat decreased MAP more in RD BPH/2J compared to sham (-12 vs -3 mmHg, P < 0.001) but had no effect in BPN/3J. RD reduced renal noradrenaline in both strains but more so in BPH/2J. RD reduced renin mRNA and protein, but not plasma renin in BPH/2J to levels comparable with BPN/3J mice. We conclude that renal nerves contribute to hypertension in BPH mice as RD induced a sustained fall in MAP, which was associated with a reduction of intrarenal renin expression. The lack of inhibition of the depressor effects of pentolinium and enalaprilat by RD suggests that vasoconstrictor effects of the SNS or RAS are not involved.
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