Angiotensin II-noradrenergic interactions in renovascular hypertensive rats.

Zimmerman, Jo B.; Robertson, David; Jackson, Edwin K.

doi:10.1172/jci113092

Cited by 35 publications

(22 citation statements)

References 26 publications

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“…This conclusion is consistent with other studies which found sympathetic hyperactivity in renovascular hypertension [36,37]. ANG II enhances the release of norepinephrine in 2K1C hypertensive rats [38] and is a primary factor in maintaining BP level after sympathectomy in rats [39]. In our study, MAP decreased in the clipped and sham-operated groups after the blockade, causing the MAP values of the groups to approach each other.…”

Section: Renal Weightssupporting

confidence: 93%

Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Özaykan

Doğan

2011

Bosn J of Basic Med Sci

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In this study, we investigated the effects of salt loading on sympathetic pressor activity, cardiac autonomic activity, mean arterial pressure (MAP), heart rate (HR) and on the relations between them in anesthetized two-kidney, one clip (2K1C) hypertensive rats. We submitted rats to either renal artery clipping or sham operation. Distilled water or 0.5 % NaCl was given orally to the clipped and sham-operated control rats for 4 weeks. Then, MAP and HR differences between pre-and post-autonomic blockade were evaluated as indexes of sympathetic pressor and cardiac autonomic activity, respectively. The autonomic blockade decreased MAP to the similar levels in all groups (between 81.7±7.6 -87.3±7.1 mmHg). Sympathetic pressor activity was greater in the clipped rats than in its sham-operated controls only under salt loading (55.3±6.2 vs. 37.0±4.1 mmHg, p<0.05). Cardiac autonomic activity was, predominantly, sympathetic and more in the clipped group than in the sham-operated rats under distilled water (48.3±8.6 vs. 19.7±7.0 beats/min, p<0.05) but not under salt loading. Salt loading inverted the relationship between HR and cardiac autonomic activity in 2K1C hypertensive rats (r=-0.76, p=0.046 vs. r=0.89, p=0.019). These results suggest that salt loading may have augmented the effect of renovascular constriction on MAP by affecting the sympathetic pressor activity and the relation between cardiac autonomic activity and HR in 2K1C hypertensive rats.

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Section: Renal Weightssupporting

confidence: 93%

Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Özaykan

Doğan

2011

Bosn J of Basic Med Sci

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“…Animals were anesthetized with pentobarbital (50 mg/kg i.p.) and were prepared for in situ perfusion of their mesenteric vascular bed as described by Jackson and Campbell 47 with the modifications of Zimmerman et al 48 Briefly, a PE 240 cannula was placed in the trachea to facilitate breathing, a jugular cannula (PE 50) was inserted for administration of supplementary anesthetic, an extracorporeal shunt was established between the abdominal aorta and superior mesenteric artery, and the mesenteric vasculature was perfused at a constant blood flow of 3 ml/min with a peristaltic pump (model 1203, Harvard Apparatus, South Natick, Mass.). All animals were treated with heparin (1,500 units) to prevent coagulation of blood in the extracorporeal shunt.…”

Section: Protocol 3: Effects Of Dup 753 and Pd123177 On The Mesenterimentioning

confidence: 99%

Effects of angiotensin subtype 1 and subtype 2 receptor antagonists in normotensive versus hypertensive rats.

1991

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“…21 There is also evidence that angiotensin II enhances norepinephrine release from mouse atria, 22 cultured adrenal medulla cells, 23 and postganglionic nerve endings. 24 Based on this evidence, it is possible that endogenous adenosine modulates catecholamine release indirectly via its effect on angiotensin II formation. In the present study, the plasma levels of epinephrine and norepinephrine in response to hydralazine-induced hypotension were significantly attenuated by captopril pretreatment.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of endogenous adenosine on epinephrine secretion from the adrenal medulla of the rat.

Tseng

et al. 1994

Hypertension

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The purpose of this study was to examine (1) whether endogenous adenosine receptors inhibit the release of epinephrine and norepinephrine from adrenal medulla in response to physiological and pharmacological stimuli and (2) whether the renin-angiotensin system modulates this effect of endogenous adenosine. We used a conscious animal model to approximate normal physiological conditions. Male Sprague-Dawley rats were treated with a surface adenosine receptor antagonist, 1,3-dipropyl-8-(p-sulfophenyl)xanthine (DPSPX) to explore the effect of endogenous adenosine. Plasma epinephrine and norepinephrine levels in response to hydralazine-induced hypotension were measured in these animals. The same protocol was repeated in rats pretreated with either adrenalectomy or captopril. The results showed that DPSPX treatment significantly increased plasma epinephrine and norepinephrine levels at both baseline conditions and after hydralazine-induced hypotension. The results from the T he endogenous nucleoside adenosine is a neuromodulator in many autonomic functions. Adenosine is known to be released by nerve terminals after depolarization.1 After release, adenosine can stimulate specific binding sites known to be coupled to adenylate cyclase.2 Adenosine is also a potent vasoactive substance known to be involved in the regulation of cerebral, 3 muscle, 4 and cardiac 5 blood flow. Our previous studies have demonstrated that endogenous adenosine plays a role in the central regulation of autonomic outflow to the cardiovascular system, 6 and antagonists such as caffeine can inhibit baroreflex activation. 7The adrenal medulla is recognized as the counterpart of postganglionic sympathetic neurons embryologically and physiologically. Both secretory cells of the adrenal medulla and postganglionic neurons are derived from the neural crest of the embryo; both are innervated by preganglionic sympathetic fibers; and both have catecholamine metabolism enzymes and release cat- © 1994 American Heart Association, Inc.adrenalectomized rats showed that the difference in plasma epinephrine level between the control and DPSPX groups originated from the adrenal medulla. Pretreatment with captopril attenuated the rise of plasma epinephrine and norepinephrine levels in DPSPX-treated animals. This result suggests that endogenous adenosine receptors inhibit epinephrine release from the adrenal medulla and suppress plasma norepinephrine levels. echolamines. Stimulation of the sympathetic nerves to the adrenal medulla causes large quantities of epinephrine and norepinephrine to be released into the circulating blood.

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Angiotensin II-noradrenergic interactions in renovascular hypertensive rats.

Cited by 35 publications

References 26 publications

Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Effects of angiotensin subtype 1 and subtype 2 receptor antagonists in normotensive versus hypertensive rats.

Modulatory effects of endogenous adenosine on epinephrine secretion from the adrenal medulla of the rat.

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