Central nervous system and the pathogenesis of hypertension. Sites and mechanisms.

Brody, Michael J.; Varner, Kurt J.; Vasquez, Elisardo C.; Lewis, Sarah

doi:10.1161/01.hyp.18.5_suppl.iii7

Cited by 78 publications

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“…3 A likely explanation for the reduced renal sympathoinhibition in DOCA-salt rats by serotonergic cardiopulmonary reflexes could be an involvement of central nervous mechanisms in the development of DOCA-salt hypertension as outlined above. 28 Interestingly, these putative central abnormalities did not influence the reflex during short-term stimulation.…”

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confidence: 90%

“…An additional explanation for the impaired volumesensitive cardiopulmonary reflexes could be that central pathways controlling efferent sympathetic activity might be affected in DOCA-salt hypertension. 28 Although the central nervous system mechanisms involved in the development of DOCA-salt hypertension are far from understood, the AV3V region close to the third ventricle and GABAergic mechanisms may play an important role.…”

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Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

et al. 1994

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We hypothesized that impaired cardiopulmonary reflexes but not altered baroreceptor reflexes precede deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats were given either DOCA and 0.9% NaCl as drinking water, 0.9% NaCl alone, or tap water. We measured mean blood pressure, heart rate, and renal sympathetic nerve activity. After 8 days, mean blood pressure was not different in DOCA-salt and control rats. Volumesensitive cardiopulmonary reflexes were tested by intravenous volume loading with saline (10% body weight in 15 minutes), which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. This response was blunted in DOCA-salt rats. Chemosensitive cardiopulmonary reflexes were tested by 15-minute infusions of the serotonin 5-HT 3 agonist phenylbiguanide, which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. Sustained decreases in A ltered central sympathetic outflow and decreased reflex control of peripheral sympathetic nerves are thought to be associated with established hypertension 14 ; however, the distinction between cause and effect is unclear. 5- 6 The sympathetic nervous system could influence blood pressure control not only by its effect on the regulation of peripheral resistance but also by controlling volume homeostasis via efferent renal sympathetic nerve activity (RSNA). -8It is well established that RSNA influences tubular water and sodium reabsorption independent of changes in intrarenal and systemic hemodynamics.2 -9 An increase in RSNA augments sodium and water reabsorption, consequently decreasing urinary flow and salt excretion. A decrease in RSNA leads to opposite effects. Thus, an impairment of RSNA regulation could alter volume homeostasis and thereby contribute to the development of hypertension. 10The activity of renal sympathetic nerve fibers is specifically controlled by cardiopulmonary reflexes. In the rat, prolonged stimulation of volume-sensitive cardiopulmonary reflexes with isotonic volume expansion inhibits RSNA but not the efferent activity of sympathetic fibers controlling peripheral resistance. -11The aim of the present study was to elucidate the putative role of these cardiopulmonary reflexes in the Received November 2, 1993; accepted in revised form June 29, 1994.From the Department of Internal Medicine, University of Erlangen-Niirnberg (Germany).Correspondence to Roland Veelken, MD, Nephrology Laboratory, Department of Medicine IV, University of Erlangen-Niirnberg, LoschgestraBe 8Vi, 91054 Erlangen, FRG.© 1994 American Heart Association, Inc.renal sympathetic nerve activity occurred during phenylbiguanide infusion in controls but were blunted over time in DOCA-salt rats. The arterial baroreflex responses to graded infusions of methoxamine and nitroprusside were analyzed by sigmoidal curve fitting. There were no differences in gain of renal sympathetic nerve activity or heart rate between the groups. Thus, DOCA-salt rats exhibit impaired cardiopulmonary ref...

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Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

et al. 1994

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“…For example, sympathetic activity increases in response to nonspecific vasodilators, whereas therapy with angiotensin-converting enzyme (ACE) inhibitors has demonstrated reduced peroneal sympathetic activity. 4 Thus, it appears that vasodilators and ACE inhibitors produce different sympathetic nerve responses; the effects of the latter could be due to either a direct-acting central mechanism 5,6 or a reduction of angiotensin II (Ang II) facilitatory effects on norepinephrine (NE) release in peripheral sympathetic nerve endings. 7,8 The aim of the present study was to assess the effect of short-term ACE inhibition on the adrenergic drive in patients with hypertension and renal artery stenosis.…”

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Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

et al. 2000

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Abstract-Hypertension with renal artery stenosis is associated with both an activated renin-angiotensin system and elevated sympathetic activity. Therefore, in this condition it may be favorable to use a therapeutic modality that does not reflexly increase heart rate, renin secretion, and sympathetic nervous activity. The purpose of the present study was to assess overall, renal, and muscle sympathetic activity after short-term administration of an angiotensin-converting enzyme inhibitor (enalaprilat) and a nonspecific vasodilator (dihydralazine) to hypertensive patients with renal artery stenosis. Forty-eight patients undergoing a clinical investigation for renovascular hypertension were included in the study. An isotope dilution technique for assessing norepinephrine spillover was used to estimate overall and bilateral renal sympathetic nerve activity. In 11 patients simultaneous intraneural recordings of efferent muscle sympathetic nerve activity were performed. Thirty minutes after dihydralazine administration, mean arterial pressure fell by 15%, whereas plasma angiotensin II, muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover increased (PϽ0.05 for all). In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (PϽ0.05). Acute blood pressure reduction by an angiotensin-converting enzyme inhibitor provokes a differentiated sympathetic response in patients with hypertension and renal artery stenosis, inasmuch that overall and muscle sympathetic reflex activation are blunted, whereas the reflex renal sympathetic response to blood pressure reduction is preserved. (Hypertension. 2000;36:543-548.)Key Words: hypertension, renovascular Ⅲ sympathetic nervous system Ⅲ renin-angiotensin system R enovascular hypertension is a condition associated with both an activated renin-angiotensin system and elevated sympathetic nerve activity. 1,2 Previous data, obtained in experimental models, indicate a positive interaction between the renin-angiotensin and the sympathetic nervous systems. 3 Therefore, in renovascular hypertension it may be favorable to use a therapeutic modality that does not reflexly further increase heart rate, renin secretion, and sympathetic nervous activity. It is well known that certain drugs used in cardiovascular medicine affect various indices of sympathetic activity. For example, sympathetic activity increases in response to nonspecific vasodilators, whereas therapy with angiotensin-converting enzyme (ACE) inhibitors has demonstrated reduced peroneal sympathetic activity. 4 Thus, it appears that vasodilators and ACE inhibitors produce different sympathetic nerve responses; the effects of the latter could be due to either a direct-acting central mechanism 5,6 or a reduction of angiotensin II (Ang II) facilitatory e...

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“…The AP functions are related with cardiovascular regulation and the catecholaminergic system as well as with the anteroventral region of the third ventricle [17,18].…”

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confidence: 99%

Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid

Carmona-Calero¹,

González-Marrero²,

Castaneyra-Martin³

et al. 2012

WJNS

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ABSTRACTand SHR were used. The paraffin sections containing the CVO were immunohistochemically processed with anti-TAp73 and by western blot, p73 bands in the CSF and circumventricular organ extract were also identified. The western blot study showed bands marked with p73 in the CSF and CVO, the p73 band expression was bigger in the SHR than in the WKY rats. We also found stronger markings in the SFO, SCO and AP of the hypertensive rats than in the WKY rats. It could be concluded that hypertension in the SHR produces alterations in the relationship between the p73 protein, circumventricular structures and CSF.

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Central nervous system and the pathogenesis of hypertension. Sites and mechanisms.

Cited by 78 publications

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Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid

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