Norepinephrine turnover in the cardiovascular tissues and brain stem of the rabbit during development of one-kidney and two-kidney Goldblatt hypertension.

Tanaka, Toshiyuki; Seki, Akira; Fujii, Jun; Kojima, Hiroshi; Ikeda, Masao

doi:10.1161/01.hyp.4.2.272

Cited by 11 publications

(9 citation statements)

References 39 publications

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“…In 2K1C hypertension, the activity of TH in proximal and distal mesenteric arteries was unchanged. This observation and the previous report of no change in NE turnover in the mesenteric artery of 2K1C hypertensive rabbits at the same time point 12 indicate the lack of a role for these sympathetic neurons in the pathophysiology of this model of hypertension. These results are compatible with the dependency of this model of hypertension on the renin-angiotensin II (Ang II) system.…”

Section: Discussionsupporting

confidence: 78%

“…The development of one-kidney, one clip (1K.1C) hypertension, a model of hypertension with a high incidence of cardiovascular complications, 5 is associated with a variety of alterations in the SNS. In this model, the cardiovascular turnover of norepinephrine (NE) is increased, 12 plasma levels of NE and its metabolites are elevated, 13 -14 and the level of NE metabolites is increased in the heart. 13 In two-kidney, one clip (2K1C) hypertension, a model with a low incidence of cardiovascular complications, 3 no alteration in SNS function is uncovered by examination of plasma levels of N E H or of the cardiovascular turnover of NE.…”

mentioning

confidence: 99%

“…13 In two-kidney, one clip (2K1C) hypertension, a model with a low incidence of cardiovascular complications, 3 no alteration in SNS function is uncovered by examination of plasma levels of N E H or of the cardiovascular turnover of NE. 12 Since SNS alterations are present in the model of hypertension with a high incidence of cardiovascular complications, these alterations may be associated with determinants for cardiovascular complications. Thus, understanding the mechanism of these alterations in the SYMPATHOADRENAL SYSTEM IN HYPERTENSION/rtaz/c/i and Campbell…”

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confidence: 99%

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Adrenal and vascular tyrosine hydroxylase activity in Goldblatt hypertension.

Rauch

Campbell

1988

Hypertension

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SUMMARY To examine the role of the sympathetic nervous system in hypertension, the in vitro activity of tyrosine hydroxylase was examined in one-kidney, one dip (1K1C) and two-kidney, one dip (2K1C) hypertensive rabbits and their respective controls 2 weeks after surgical procedures. The in vitro activity of tyrosine hydroxylase provides a measure of catecholamine synthesis and serves as a biochemical index of activity of noradrenergic neurons and the adrenal medulla. Mean arterial pressure rose from 91.5 ± 1.0 to 125.5 ± 5.6 mm Hg (p < 0.01) in the 1K1C group and from 91.8 ± 1.3 to 106.5 ± 5.0 mm Hg (p < 0.02) hi the 2K1C group, whereas no change in blood pressure was found in their respective controls. Adrenal tyrosine hydroxylase activity was increased 85% in the 1K1C group, as compared with values in one-kidney controls (from 11.8 ± 1.5 to 21.8 ± 1.1 pmol COj/mln/mg; p < 0.0002), and was increased 49% in the 2K1C group, as compared with values in two-kidney controls (from 8.01 ± 1.2 to 11.9 ± 1 . 1 pmol COj/min/mg; p < 0.02). In the 1K1C group, proximal mesenteric tyrosine hydroxylase activity was decreased 46% compared with values in one-kidney controls (from 23.5 ± 5.0 to 12.8 ± 2.5 pmol CO]/ min/mg; p < 0.03) and distal mesenteric tyrosine hydroxylase activity was decreased 42% (from 7.73 ± 1.2 to 4.46 ± 0.8 pmol COj/mln/mg; p < 0.03). In the 2K1C group, neither proximal nor distal mesenteric tyrosine hydroxylase activity was altered. Tyrosine hydroxylase activity was not detectable in the femoral arteries, or hi the thoracic and abdominal aorta. These results indicate that the adrenal medulla contributes to the patbophysioJogy of both 1K1C and 2K1C forms of hypertension. These results also indicate that alterations hi the sympathetic nervous system in 1K1C hypertension are not mediated by an activation of tyrosine hydroxylase in the mesenteric arteries. of diseases that are collectively characterized by an elevated systemic blood pressure. Efforts to reduce the risk of cardiovascular complications in hypertension have focused on the treatment of the elevated blood pressure; however, blood pressure is not the sole determinant for cardiovascular complications in hypertension.1 In experimental models of hypertension, the elevation in blood pressure cannot predict the occurrence of necrotizing arteritis 2 -3 and cerebral hemorrhages 6 or the degree of vascular 3 -7 and cardiac hypertrophy. 8 -1 ' The identity of other determinants for cardiovascular complications in experimental models of hypertension is unknown. Identification of these determinants would aid not only in understanding the pathogenesis of cardiovascular disease but also in developing more efficacious treatments for hypertension. The sympathetic nervous system (SNS) participates in the regulation of blood pressure and plays a key role in the pathophysiology of hypertension. The development of one-kidney, one clip (1K.1C) hypertension, a model of hypertension with a high incidence of cardiovascular complications, 5 is associated with a variety ...

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Section: Discussionsupporting

confidence: 78%

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confidence: 99%

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confidence: 99%

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Adrenal and vascular tyrosine hydroxylase activity in Goldblatt hypertension.

Rauch

Campbell

1988

Hypertension

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“…Using a biochemical marker, Tanaka et al have shown that noradrenaline turnover in the aorta, mesentery, and heart are the same in 2K1C rabbits compared with normotensive controls. 12 Furthermore, the hypotension to ganglionic blockade is much greater in renovascular hypertension, suggesting that the effect we are seeing with rilmenidine reflects an effect on most if not all sympathetic beds. Results from a "within-patient" study, before and 12 months after reversal of renovascular hypertension, showed no change in total noradrenaline spillover, suggesting that the hypertension did not elevate global sympathetic activity.…”

Section: Head and Burke Sympathetic Responses In Hypertensive Rabbitsmentioning

confidence: 89%

“…9,11 Reports of noradrenaline turnover in 2K1C rabbits have found no change in turnover from a range of tissues suggesting that there is not a generalized change in sympathetic activity in this model. 12 Thus there is a paradox. How can the contribution of the sympathetic nervous system increase if the level of activity stays the same?…”

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confidence: 99%

Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Head

Burke

2004

Hypertension

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Abstract-We determined whether the sympathetic excitatory responses to environmental stressors and the sympathoinhibitory responses to rilmenidine are altered by renovascular hypertension. Rabbits were made hypertensive with a clip on the right renal artery, and a left renal nerve recording electrode was implanted. After 3 or 6 weeks, the animals were given air-jet stress and loud noise stress before and after intravenous rilmenidine. Three and 6 weeks after renal clipping, mean arterial pressure was 28% and 36% greater than preclip values. Air-jet stress elicited a marked increase in renal sympathetic nerve activity, mean arterial pressure, and heart rate. Renal sympathetic nerve activity responses were much greater in hypertensive rabbits, but the pressor responses were similar to those observed in normotensive animals. Acute administration of rilmenidine decreased blood pressure more in hypertensive animals but with a much lesser inhibition of sympathetic activity. Rilmenidine markedly reduced increased sympathetic activity during air-jet stress in 3-week clipped rabbits but to a lesser extent in the other groups. These studies show that while sympathetic responses to stress were markedly enhanced in renal clip hypertensive rabbits, they did not result in greater pressor responses, thus suggesting that vascular neuroeffector mechanisms were not altered. By contrast, the increased effects of rilmenidine suggest a much greater contribution to the hypertension by the sympathetic nervous system, but one that is caused by an enhanced "nonvascular" neuroeffector mechanism. As such, sympathoinhibitory agents such as rilmenidine are very suitable and very effective agents for the treatment of renovascular hypertension. Key Words: renal nerves Ⅲ hypertension Ⅲ stress Ⅲ sympathetic nervous system Ⅲ rabbits Ⅲ blood pressure Ⅲ heart rate T here has been a long-standing interest in the role of the sympathetic nervous system in hypertension, but more so in view of increasing evidence that it can contribute to the long-term setting of blood pressure. 1 In renovascular hypertension, there is much evidence for a greater dependence of the hypertension on the sympathetic nervous system. 2 A greater depressor response to ganglion blockade has been observed in renal wrap hypertensive rats. 3 Studies in the rabbit by Cox and Bishop showed that during angiotensin (Ang) infusion, the hypertension was initially caused by Ang-mediated vasoconstriction that subsided and was replaced by a greater neurogenic component. 4 One of the major difficulties in determining the contribution of the sympathetic nervous system in hypertension has been in making direct comparisons of microvolt values between different groups. Recently, we developed a novel method for comparing sympathetic activity between groups of animals 5 and found that renal sympathetic nerve activity (RSNA) is not increased but initially decreased or unchanged in 2-kidney 1-clip (2K1C) hypertensive rabbits. 6 Studies in renal wrap 7 and chronic Ang-induced hypertension 8 support...

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Mechanisms of Experimental and Human Renovascular Hypertension

Salazar¹,

Quesada²

1992

Renovascular and Renal Parenchymatous Hypertension

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Norepinephrine turnover in the cardiovascular tissues and brain stem of the rabbit during development of one-kidney and two-kidney Goldblatt hypertension.

Cited by 11 publications

References 39 publications

Adrenal and vascular tyrosine hydroxylase activity in Goldblatt hypertension.

Adrenal and vascular tyrosine hydroxylase activity in Goldblatt hypertension.

Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Mechanisms of Experimental and Human Renovascular Hypertension

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