Role of angiotensin II and catecholamines in blood pressure variability responses to stress in SHR

Gaudet, E; Blanc, Jocelyne; Elghozi, Jean‐Luc

doi:10.1152/ajpregu.1996.270.6.r1265

Cited by 16 publications

(13 citation statements)

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“…This does not occur when the SNS is most active (during the night). Similarly, Gaudet et al [41] have shown that the combination of a 1 -adrenoreceptor and chronic AT 1 -receptor blockade by losartan was more hypotensive compared with the effect of prazosin alone in WKY rats and SHRs. They suggested that the chronic inhibition of the RAS led to increased sympathetic tone [41].…”

Section: Discussionmentioning

confidence: 79%

Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Palma‐Rigo

Jackson

Davern

et al. 2011

Journal of Hypertension

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The hypotensive actions of losartan suggest that although the RAS provides an important contribution to BP, it contributes little, if at all, to the hypertension-induced or the greater stress-induced pressor responses in Schlager mice. The effects of pentolinium suggest that the SNS is mainly responsible for hypertension in BPH/2J mice. However, the RAS inhibits sympathetic vasomotor tone during inactivity and prolongs sympathetic activation during periods of adverse stress, indicating an important sympatho-modulatory role.

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Section: Discussionmentioning

confidence: 79%

Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Palma‐Rigo

Jackson

Davern

et al. 2011

Journal of Hypertension

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“…The reason is twofold. First, effects of air-jet stress on fast rhythms of AP have been thoroughly described in rats (2,4,12). Secondly, an increased sympathetic baroreflex gain is expected to attenuate low and very low frequency components of AP variability (5,15).…”

Section: Discussionmentioning

confidence: 99%

Baroreflex control of renal sympathetic nerve activity during air-jet stress in rats

Kanbar

Oréa²,

Barrès³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Kanbar R, Oréa V, Barrès C, Julien C. Baroreflex control of renal sympathetic nerve activity during air-jet stress in rats. Am J Physiol Regul Integr Comp Physiol 292: R362-R367, 2007. First published September 14, 2006; doi:10.1152/ajpregu.00413.2006.-The effects of acute emotional stress on the sympathetic component of the arterial baroreceptor reflex have not yet been described in conscious animals and humans. Arterial pressure (AP) and renal sympathetic nerve activity (RSNA) were simultaneously recorded in 11 conscious rats before and during exposure to a mild environmental stressor (jet of air). Baroreflex function curves relating AP and RSNA were constructed by fitting a sigmoid function to RSNA and AP measured during sequential nitroprusside and phenylephrine administrations. Stress increased mean AP from 112 Ϯ 2 to 124 Ϯ 2 mmHg, heart rate from 381 Ϯ 10 to 438 Ϯ 18 beats/min, and RSNA from 0.80 Ϯ 0.14 to 1.49 Ϯ 0.23 V. The RSNA-AP relationship was shifted toward higher AP values, and its maximum gain was significantly (P Ͻ 0.01) increased from 9.0 Ϯ 1.3 to 16.2 Ϯ 2.1 normalized units (NU)/mmHg. The latter effect was secondary to an increase (P Ͻ 0.01) in the range of the RSNA variation from 285 Ϯ 33 to 619 Ϯ 59 NU. In addition, the operating range of the reflex was increased (P Ͻ 0.01) from 34 Ϯ 2 to 41 Ϯ 3 mmHg. The present study indicates that in rats, the baroreflex control of RSNA is sensitized and operates over a larger range during emotional stress, which suggests that renal vascular tone, and possibly AP, are very efficiently controlled by the sympathetic nervous system under this condition. arterial pressure; baroreceptor reflex; gain; sympathetic nervous system IN LABORATORY ANIMALS AND human subjects, emotional stress evokes parallel increases in arterial pressure (AP), heart rate (HR), and sympathetic nerve activity (SNA) (1, 2, 17). In sleeping or quiet resting subjects, pharmacologically induced increases in AP result in reflex decreases in HR and SNA. From this simple observation, it is logical to hypothesize that emotional stress inhibits or even suppresses the arterial baroreceptor reflex. Support to this hypothesis came initially from studies performed on anesthetized animals. Specifically, electrical stimulation of the hypothalamic defense area of cats, which mimics the cardiovascular and autonomic effects of emotional stress (8), was shown to inhibit baroreceptive neurons in the nucleus tractus solitarius (22). In the latter study, however, it could not be excluded that electrical stimulation had activated fibers of passage. Therefore, the question was recently revisited by using a pharmacological approach. It was found that in urethane-anesthetized rats, disinhibition of neurons of the defense area with a GABA A receptor antagonist induced a rightward shift of the renal SNA (RSNA) baroreflex function curve and increased its sensitivity (20).It is amazing that the effects of emotional stress on the characteristics of the sympathetic baroreceptor reflex have not yet been reported. Howe...

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“…Immediately afterward, an additional catheter was inserted into the femoral artery of all animals, as described in ref. 31, for continuously recording arterial BP. The catheters were tunneled s.c. to exit from the neck.…”

Section: Methodsmentioning

confidence: 99%

Brain renin-angiotensin system blockade by systemically active aminopeptidase A inhibitors: A potential treatment of salt-dependent hypertension

Fournié‐Zaluski

Fassot

Valentin

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

121

131

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The hyperactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several types of experimental and genetic hypertension animal models. We previously reported that in the murine brain, aminopeptidase A (APA) is involved in the conversion of angiotensin II (AngII) to AngIII and that AngIII is one of the main effector peptides of the brain RAS in the control of vasopressin release. Here we report that brain AngIII exerts a tonic stimulatory effect on blood pressure in a model of salt-dependent hypertension, the DOCA-salt rat, characterized by a depressed systemic but a hyperactive brain RAS. Similar high blood pressure accompanied by a low systemic renin state was described in some patients, especially in hypertensive African Americans who are resistant to treatment by blockers of the systemic RAS. We developed RB150, a prodrug of the specific and selective APA inhibitor, EC33. RB150 given i.v. is able to cross the blood-brain barrier, to inhibit brain APA, and to block the formation of central AngIII. A single dose of systemic RB150 (15 mg͞kg, i.v.) in conscious DOCA-salt rats inhibited brain APA activity and markedly reduced blood pressure for up to 24 h. These results demonstrate the crucial role of brain APA as a candidate target for the treatment of hypertension and suggest that RB150, a potent systemically active APA inhibitor, could be the prototype of a new class of antihypertensive agents for the treatment of certain forms of hypertension.

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Role of angiotensin II and catecholamines in blood pressure variability responses to stress in SHR

Cited by 16 publications

References 0 publications

Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Baroreflex control of renal sympathetic nerve activity during air-jet stress in rats

Brain renin-angiotensin system blockade by systemically active aminopeptidase A inhibitors: A potential treatment of salt-dependent hypertension

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