Norepinephrine kinetics in dogs with experimentally induced renal vascular hypertension

Buranakarl, Chollada; Benjanirut, Chutamas; Pondeenana, S.; Bovée, Kenneth C.

doi:10.2460/ajvr.2000.61.1534

Cited by 4 publications

(3 citation statements)

References 39 publications

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“…Since the pioneering work of a canine model of renal vascular hypertension was reported by Goldblatt et al 8 many methods, for example, the snare, 5–17 cuff, 18 or single-hole clip, 19 have been used to induce hypertension in large animals for different purposes. However, few of these methods have been used to induce arterial plaque formation.…”

Section: Discussionmentioning

confidence: 99%

Carotid Proliferative Plaque Formation in a Canine Model of Chronic Hypertension

Tian¹,

Shen²,

Liao

et al. 2013

Journal of Investigative Medicine

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Section: Discussionmentioning

confidence: 99%

Carotid Proliferative Plaque Formation in a Canine Model of Chronic Hypertension

Tian¹,

Shen²,

Liao

et al. 2013

Journal of Investigative Medicine

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“…In rats both one-kidney, oneclip and two-kidney, one-clip hypertension are associated with elevated plasma norepinephrine levels [65]. In twokidney, two-clip hypertensive dogs, plasma catecholamine concentrations and norepinephrine spillover rate were significantly increased [66]. Based on MSNA recordings and measurements of total body norepinephrine spillover several [67 -69] but not all studies [27] found elevated sympathetic activity in patients with renovascular hypertension.…”

Section: Renovascular Hypertension and Angiotensin IImentioning

confidence: 98%

Interactions between the sympathetic nervous system and the kidneys in arterial hypertension

Grisk

Rettig

2004

Cardiovascular Research

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Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Principles of sympatho-renal interactions in chronic hypertension are reviewed. Alterations in the ontogeny of the sympathetic nervous system and the kidney, inherited abnormalities in sensory receptor function and exaggerated responsiveness to mental stress contribute to inappropriately high sympathetic activity in primary or essential hypertension. Careful characterization of clinical study populations shows that elevated sympathetic activity and "essential" hypertension are not unequivocally associated. Prospective clinical studies which investigate a broader array of physiological functions and experiments in recombinant inbred rodents with less traumatic nerve recording techniques than currently available will help to define under which conditions elevated sympathetic activity is indeed a cause of primary hypertension. Signals arising from the kidney which activate the renin-angiotensin system and afferent renal nerves increase sympathetic activity. These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease.

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“…The extracellular volume expansion induced by anuria is the main pathophysiological determinant of hypertension in hemodialysis patients (10). In addition, the norepinephrine concentration in dogs with experimentally induced renal vascular hypertension tends to increase (11). Therefore, it seems likely that hypertension in renal dysfunction dogs was induced by extracellular volume expansion and changes in sympathetic nervous activity.…”

mentioning

confidence: 99%

Effects of a Selective Inhibitor of Inducible Nitric Oxide Synthase, ONO-1714, on Experimental Hemodialysis-Related Hypotension in Renal Dysfunctional Dogs

et al. 2004

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Abstract. The effect of a selective inducible nitric oxide synthase inhibitor, ONO-1714 ((1S,5S,6R,7R)-7-chloro-3-imino-5-methyl-2-azabicyclo[4.1.0]heptane hydrochloride), on hemodialysis-related hypotension was investigated using a canine model of renal dysfunction. Renal dysfunction was induced in dogs by complete bilateral ligation of renal arteries. On performing hemodialysis with ultrafiltration, the blood pressure of the renal dysfunction dogs gradually decreased and persisted at reduced levels until completion. ONO-1714 ameliorated the hemodialysis-induced hypotension in the renal dysfunction dogs at a dose that did not influence blood pressure in non-hemodialysis dogs with normal renal function. The above findings indicated that ONO-1714 may elicit beneficial effects on hemodialysis-related hypotension.

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Norepinephrine kinetics in dogs with experimentally induced renal vascular hypertension

Cited by 4 publications

References 39 publications

Carotid Proliferative Plaque Formation in a Canine Model of Chronic Hypertension

Carotid Proliferative Plaque Formation in a Canine Model of Chronic Hypertension

Interactions between the sympathetic nervous system and the kidneys in arterial hypertension

Effects of a Selective Inhibitor of Inducible Nitric Oxide Synthase, ONO-1714, on Experimental Hemodialysis-Related Hypotension in Renal Dysfunctional Dogs

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